Test 1, Deck 2 Flashcards
Refractory characteristics of slow vs fast APs
slow- time dependent- Ca2+ - longer
fast- voltage dependent- Na+
R on T phenomenon- PVCs
a premature beat (R wave) occurs during the relative refractory period of the previous beat (T wave)
aka premature ventricular contraction
- PVCs= polymorphic ventricular tachycardia
what is special about the refractory period of the AV node
have post-repolarization refractoriness
- protects the ventricles during atrial fibrilation
- depends on Ca2+ channels
In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation?
AV node refractory characteristics
How do you slow ventricular rate in patient with atrial fibrilation?
Calcium channel blocker or Beta blocker
as HR goes up, which part of the cardiac cycle shortens most
diastole
action potential duration equals what part of the cardiac cycle and what part of the EKG
systole
Q-T
what causes prolonged Q-T syndrome (T wave is super late)
acquired- bradycardia, hypokalemia, quindine
congenital- defects in sodium and potassium channels
e.g. Torsades (doesn’t repolarize normally is AP is too long, can be initiated by R on T)
hierarchy of cardiac pacemaker activity
arranged based on inherent beating rate:
SA node > latent atrial pacemakers > AV nodal/His bundle (junctional) > bundle branches > Purkinje’s
diastolic depolarization- SA node
- T-type Ca current (at - voltages, Ca in)
- hyperpolarization-activated inward current od sodium (funny channels)
- deactivation of K+ current
- inward Na/Ca exchanger
diastolic depolarization- Purkinje fibers
- hyperpolarization-activated inward current of sodium (funny channels)
- deactivation of K+ current
things that change heart rate
1- slope of diastolic depolarization
2- change in maximum diastolic potential (resting potential)
3- change in threshold
4- change of pacemaker
how would vagal nerve stimulation affect an EKG recording?
would have a longer R-R (less bpm)
what is sinus arrhythmia
variability in pacemaker cycle length caused by respiratory changes
inspiration- increase HR- inhibits PS nerve activity
expiration- decreases HR- stimulate PS nerve activity
heart rate is slower during expiration/inspiration
expiration
molecular reasons for cardiac arrhythmia
impulse formation, conduction, or both
electrical mechanisms responsible for dysrhythmias
altered automaticity, re-entry of excitation, triggered activity
causes of tachy-dysrhythmias
NE (sympathetics)
stimulants (caffeine)
stretching (aneurism)
sick sinus syndrome, fever, hyperthyroidism (BUSH)
causes of brady-dysrhythmias
drugs (beta blockers, calcium channel blockers, digitalis) barbiturates, anesthetics ishchmia/infarct sick sinus syndrome aging
causes of re-entry excitations
ischemia
infarction
congenital bypass tracts (WPW)
causes of DADs
"Delayed afterdepolarization" digitalis elevated catecholamines rapid heart beat EVERYTHING TOGETHER
causes of EADs
"Early after depolarization" acidosis (ischemia) hypokalemia quinidine slow heart rates
3 requirements for re-entry of excitation
1- geometry for conduction loop
2- slow or delayed conduction
3- unidirectional conduction block
anti-arrhythmic therapies
1- drugs (Ca channel blockers, beta blockers)
2- radio frequency ablation
3- DC cardioversion
4- implantable cardioverter-defibrillator
PR interval length
0.12-0.2 seconds
QRS complex length
0.07-0.1 seconds
QT interval length
0.25-0.43 seconds
cardiac E-C coupling steps (CICR)
1) AP goes down into T-tubules
2) Depolarization activates L-type Ca2+ currents on sarcolemma & t-tubule membrane
3) Influx of Ca2+ binds to SR and opens Ryr channels
4) Released Ca2+ binds to troponin C
5) Relaxation occurs when Ca2+ is removed
structure-function EC coupling: sarcolemma
- propagates action potentials
- controls Ca2+ influx via slow inward Ca2+ current
structure-function EC coupling: T-tubules
- transmits electrical activity to cell interior
- located at Z-lines
structure-function EC coupling: SR, terminal cisternae
- where Ca2+ influx triggers opening of Ca2+ release channels
structure-function EC coupling: SR, longitudinal cisternae
- cite of Ca2+ re-uptake to initiate relaxation
structure-function EC coupling: troponin C
- Ca2+ receptor on actin (contractile protein)
cardiac vs skeletal muscle: size, connection, activation
size: cardiac are much smaller
connection: cardiac are electrically coupled (syncytium) vs individual muscle cells
activation: cell to cell conduction vs Ach transmission at NMJs
cardiac vs skeletal muscle: contraction, contraction amplitude, summation, metabolism
contraction: CICR vs voltage-sensors on Ca2+ channels
amplitude: Ca2+ influx and SR content vs frequency of APs
summation: no summation vs tetanus
metabolism: aerobic (35%mit) vs anaerobic (2% mit)
what is contractility, and can you change the strength of a contraction without changing it?
contractility- the inherent ability of actin and myosin to form cross-bridges and generate contractile force; determined by intracellular Ca2+
YES
what are catecholamines
NE (neurotransmitter) and E (hormone)
mechanism of catecholamines
1) bind to Beta1 receptors on sarcolemma
2) activation adenyl cyclase to increase cAMP
3) cAMP activates PKA
4) PKA phosphorylates lots of stuff
what does PKA phosphorylate in the catecholamine cascade?
1- Ca2+ channels- increases calcium influx
2- phospholamban- increases SRCA rate (relaxation)
3- troponin I- reduces troponin C’s affinity for calcium
1&2 increase strength of contraction
2&3 decrease time course of relaxation
mechanism of calcium channel blockers
1- plugs up Ca+ influx
2- decreases SR release of Ca2+- leads to less contraction (VASODILATION)
3- inhibition of slow inward Ca2+ channel inhibits conduction of AV node, blocks SVT
3 factors that change muscle contraction via a change in contractility
1) catecholamines- sympathetics
2) cardiac glycosides (dig)
3) Ca2+ channel blockers (vasodilator, blocks SVT)
Cycle length influences contraction amplitude by altering _______ by altering the time available for intracellular Ca2+ handling
contractility
positive staircase- as heart rate increases, the strength of the contraction ____
increases
- greater Ca2+ influx at higher HR, less time for Ca2+ efflux; increased SR content and release
premature beat results in a ___ than normal contraction
smaller
- less time for recovery of slow inward Ca2+ current & SR release channels & re-organization of terminal cisternae
- gives you a smaller CICR release
what is a PESP
post-extrasystolic potentiation
- stronger than normal contraction of the heart following a premature beat
- more time for recovery of Ca2+
signs of A-fib w/ radial pulse
fast heart rate (tachycardia), irregular speed of heart rate, force for each beat is different
- because of force-frequency relationship, different amounts of Ca2+ causing different forces of contraction
- skipped beat is b/c not enough pressure to open aortic valve
- thumping is a PESP
contractility of the heart is ____ with a premature beat
reduced
turn on an electric stimulator (in a lab) to increase heart rate, what does it look like?
premature beat (but think stair-case effect- slowly recovers)
four factors that determine cardiac output
1) heart rate
2) myocardial contractility
3) preload
4) afterload
what is preload dependent on?
if preload were low, what would the treatment be?
- end-diastolic volume (the amount of ventricular filling)
- generates passive tension
- give more volume
afterload is any force that _____
resists muscle shortening e.g. arterial pressure
the load on the muscle after contraction is initiated
a premature beat is a _____ contraction
isometric
if compliance is low, the tissue is _____; aka _____
stiff; heart
the slope of the resting tension curve is primarily determined by
muscle compliance
the slope of the active tension curve is primarily determined by
muscle contractility
what is resting diastolic tension
the amount of tension that develops passively by stretching the muscle (increasing preload)
initial myocardial fiber length= EDV
what is active systolic tension
the amount of isometric tension that is developed by muscle contraction at a particular preload
stretching cardiac muscle …
a) creates more optimal overlap between the thick and thin filaments
b) increases Ca2+ sensitivity of myofilaments
_____ increases the max slope of the systolic tension curve, and _____ decreases it
sympathetics; heart failure
an increase in preload ____ the amount of muscle shortening
increases
an increase in afterload ___ the amount of muscle shortening
decreases
A positive increase in contractility changes what? (tension, relaxation, muscle shortening, velocity of shortening)
- raises peak isometric tension
- enhances the rate of relaxation (sympathetics)
- increases the amount of muscle shortening
- increases the velocity of shortening
afterload is synonymous with what
force
increasing afterload
decreases the velocity of muscle shortening
decreases the amount of muscle shortening
at a given afterload, an increase in preload
shifts the curve right; increases the velocity of shortening and the max isometric force
at a given afterload, an increase in contractility
shifts the curve up and to the right; increases the velocity of shortening and the max isometric force
EKG inferior view of the heart
leads 2, 3 and aVF
EKG lateral view of the heart
leads 1, aVL, V5, V6
EKG anterior view of the heart
leads V3, V4
EKG septal view of the heart
leads V1, V2
which electrode is most parallel to mean frontal plane vector? and which direction is it in?
II, down and left
order of ventricular depolarization
interventricular septum (down-right), apical depolarization (down-left), endocardial surface (down-left)
why is the vector of repolarization the same as depoarlization?
- repo starts where depo ends
- repo goes from positive to negative, so vector is switched
what is the last part of the heart to depolarize?
epicardial surface of the left ventricle
where is the AP slower- endo or epi- and why?
endocardial surface- it has less Ito K+ channels, repolarization takes longer
normal angles for Einthoven’s triangle
-30* - 105*
if the mean frontal plane vector is more negative than -30, which kind of deviation is it?
left axis
how to use hexaxial reference to approximate the MFPV
1- pick smallest recording of the 12
2- take line perpendicular to that
3- see if that line is + or - (pointing right or left)
4- use that line to approximate vector
einthoven triangle method
1- sum blocks up and down for q+rs+t for two leads (1+3=2)
2- plot value on triangle
things that skew MFPV
left ventricular hypertrophy
pulmonary hypertension
bundle branch block (right deviation w/ right block)
which part of conduction does hypokalemia affect most and what happens?
Purkinje fibers- AP lengthens and u wave pops out
U wave- after T, repolarization of purkinjes
if all the QRS complexes are taller, what do you suspect?
hypertrophy- more cells= more current
phases of the cardiac cycle
atrial systole (last squeeze) isovolumic contraction (**all valves closed) ejection- rapid and reduced isovolumic relaxation filling- rapid & reduced
units for pressure, aortic blood flow, ventricular volume, time
mm Hg (0-120)
L/min (0-5)
ml (20-38)
0-0.8 seconds
ACV waves
A- atrial contraction
c- ventricular contraction
v- filling & emptying of atrial chamber
3rd heart sound
rapid filling of blood into a heart that dilated
4th heart sound
vigorous contraction of atria pumping into ventricle
systolic murmur
- stenosis of aortic/pulmonic valve
or - insufficient/incompetent mitral/tricuspid valve
diastolic murmer
-stenosis of mitral/tricuspid valve
or
-insufficient aortic/pulmonic valve
physiological splitting
Aortic valve followed by pulmonic valve during inspiration (negative pressure caused by inspiration pulls right ventricle out, filling takes longer- negative pressure differential; more preload)
paradoxical splitting
Pulmonic followed by aortic due to left bundle branch block (come closer together during inspiration)
persistent splitting
right bundle branch block- becomes exaggerated with inspiration
- cardiac index and units
- venous pressure
- 2.5-4.0 (3.1)
litres/min/sq m - 3-8 mm Hg
right atrial pressure
right ventricle pressure (systolic)
right ventricle pressure (end-diastolic)
-2-5 (2)
18-30 (25)
-5-5 (2)
Pulmonary artery systolic, diastolic, mean
18-30 (25)
6-12 (10)
10-20 (15)
Pulmonary wedge pressure
left atrial pressure
0-12 (6)
left ventricle- systolic
left ventricle- diastolic
100-140 (120)
85-105 (95)
