4. Physiology II - Conducting System Flashcards
what BEGINS the CARDIAC CYCLE (at end of diastole) what causes ATRIA to CONTRACT after passive filling
SINO-ATRIAL NODE FIRES (DEPOLARISES)
spreads wave of depolarisation through right atrium and to left atrium
-> ATRIA CONTRACT
(15% ventricular filling)
what happens as the CONDUCTION / wave of DEPOLARISATION PASSES through the AV NODE
DELAYS it - slows down before reaching Bundle of His, Bundle Branches, Purkinje Fibres
allows time for atria to move blood out through valves before the ventricles contract (so atria and ventricles don’t contract simultaneously)
how are IMPULSES in SYSTOLE (ventricular contraction)
RAPID TRANSMISSION through VENTRICLES
- COORDINATED VENTRICULAR CONTRACTION
(radially, longitudinally and twisting motion)
SPECIFIC ACTIVATION SEQUENCE to OPTIMISE EJECTON of blood
(bundle branch block is dangerous)
in what direction are VENTRICULAR CONTRACTIONS to OPTIMISE ejection of blood
RADIALLY (side to side)
LONGITUDINALLY (from apex to base)
and TWISTING MOTION
what is POLARISATION
a DIFFERENCE in CHARGE between sides of a MEMBRANE
if something is POLARISED what does it mean
INSIDE MORE NEGATIVE
if something is DEPOLARISED what does it mean
INSIDE MORE POSITIVE
what is VOLTAGE
the DIFFERENCE in POSITIVE CHARGES from one side of a membrane to the other
(-80mV in myocytes, resting)
what is a CURRENT
the FLOW of CHARGED PARTICLES ACROSS a MEMBRANE
how are CARDIAC MYOCYTES at REST (resting potential)
POLARISED (inside Negative)
at - 80mV
due to K+ EFFLUX (out of cells)
how do CURRENTS PASS BETWEEN MYOCYTES (excite each other)
via GAP JUNCTIONS
when can MYOCYTES REGAIN EXCITABILITY
ONLY when FULLY REPOLARISED
what is REFRACTORY PERIOD
period of TIME during which a second STIMULUS will FAIL to GENERATE a 2ND ACTION POTENTIAL in a myocyte
- as cannot generate 2nd action potential unless fully repolarised
how do PARTICLES travel into cells (by what gradients)
DOWN ELECTRO-CHEMICAL GRADIENT
- CHEMICAL gradient
- ELECTRICAL gradient for CHARGED particles
What is a REVERSAL POTENTIAL
when ELECTROCHEMICAL GRADIENT is BALANCED
(inward and outward forces are equal / eventually reach equilibrium)
name of the EQUATION that PREDICTS WHERE the REVERSAL POTENTIAL will lie / where the ELECTROCHEMICAL GRADIENT WILL BALANCE
NERNST EQUATION
what CHANNELS should we OPEN if we want to make MEMBRANE REVERSAL POTENTIAL LOWER / MORE NEGATIVE, as they have really negative reversal potential
K+ CHANNELS
(-95mV reversal potential)
what CHANNELS should we OPEN if we want to make MEMBRANE REVERSAL POTENTIAL HIGHER / MORE POSITIVE, as they have high reversal potential
Na+ CHANNELS
(+55mV reversal potential)
types of ION CHANNELS in cardiomyocytes
VOLTAGE GATED
- activation gate opens when membrane potential becomes more positive
- are TIME DEPENDENT
LIGAND GATED
by chemical (ie Ach) or mechanical (stretch)
what channel uses ATP in cardiomyocytes
NA/K PUMP
3 Na+ OUT
2 K+ IN
(restore balance)
(electrogenic, creates current)
what TRANSPORTER is used in cardiomyocytes
NA/CA EXCHANGER
1 Ca2+ OUT (CALCIUM EFFLUX)
exchanged for
3 Na+ IN
- PASSIVE, no ATP
can also work in reverse for Calcium Influx
- electrogenic, creates current
what is the RESTING POTENTIAL and how is this GENERATED
-80 mV
- K+ EFFLUS as K+ CHANNELS OPEN in resting state
stages of an ACTION POTENTIAL GENERATION that make the SPIKE AND DOME MORPHOLOGY
- RAPID Na+ INFLUX as Na+ channels OPEN
(exceeds threshold) - K+ CHANNELS OPEN, K+ EFFLUX
- Ca2+ CHANNELS OPEN, Ca2+ INFLUX (makes plateau as balances K+ efflux)
- Ca2+ CHANNELS CLOSE
- REPOLARISATION (flat)
ACTION POTENTIAL CREATED by the FLOW of which ION(S)
-
CHANNELS used to CREATE ACTION POTENTIALS
- Na+ CHANNEL (Na+ in)
- K+ CHANNEL (K+ out)
- Ca2+ CHANNEL (Ca2+ in)
- NA/K ATPase (Na+ out, K+ in)
- NA/Ca EXCHANGER (Na+ in, Ca2+ out)
how does Na+ TRAVEL when Na+ CHANNEL is OPEN
IN
how does K+ TRAVEL when K+ CHANNEL is OPEN
OUT
how does Ca2+ TRAVEL when Ca2+ CHANNEL is OPEN
IN
how does Na+ TRAVEL through NA/K PUMP
OUT (3)
how does K+ TRAVEL through NA/K PUMP
IN (2)
how does Na+ TRAVEL through NA/CA EXCHANGER
IN
how does Na+ TRAVEL through NA/CA EXCHANGER
IN (3)
how does CA2+ TRAVEL through NA/K PUMP
OUT (1)
INFLUX of …. leads to MYOCYTE CONTRACTION
CALCIUM
what happens in PHASE 0 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY
RAPID UPSTROKE
(Na+ influx)
what happens in PHASE 1 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY
INITIAL REPOLARISATION
(K+ efflux)
what happens in PHASE 2 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY
PLATEAU
(Ca+ influx and K+ efflux BALANCE)
what happens in PHASE 3 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY
FINAL REPOLARISATION
(K+ efflux)
what happens in PHASE 4 of CARDIOMYOCYTE ACTION POTENTIAL in SPIKE AND DOME MORPHOLOGY
STRONGLY POLARISED
almost FLAT RESTING POTENTIAL
how are ACTION POTENTIALS from ATRIAL MYOCYTES
SHORTER DURATION
lower plateau
the SINO-ATRIAL NODE (SAN) ACTION POTENTIAL is adapted to FUNCTION as a …
PACEMAKER
how is PHASE 0 of SAN ACTION POTENTIAL
SLOW UPSTROKE
- less steep
how is PHASE 4 of SAN POTENTIAL
LESS POLARISED (moderately)
UPSLOPING RESTING POTENTIAL, NOT FLAT
- SLOWLY DEPOLARISING
CARDIAC CONDUCTION is LARGELY CONTROLLED by … TONE
AUTONOMIC TONE
impact of SYMPATHETIC TONE on HEART RATE (chronotropy), SPEED of conduction (dromotropy) and FORCE of contraction (inotropy)
INCREASES HEART RATE, CONDUCTION SPEED, FORCE
impact of PARASYMPATHETIC TONE on HEART RATE (chronotropy), SPEED of conduction (dromotropy) and FORCE of contraction (inotropy)
DECREASES HEART RATE, CONDUCTION SPEED, FORCE
what NERVE STIMULATION SLOWS HEART RATE
VAGAL NERVE stimulation
DRUG that can SLOW HEART RATE by BLOCKING SYMPATHETIC TONE
(increase RR intervals - time between systoles)
BETA BLOCKERS ie PROPANOLOL
DRUG that can INCREASE HEART RATE by BLOCKING PARASYMPATHETIC TONE
(decreases RR intervals - time between systoles)
ATROPINE
PROPANOLOL BLOCKS…
SYMPATHETIC TONE and thus SLOWS HEART RATE
HEART RATE is MODULATED by VARYING the SLOPE of … of the SAN ACTION POTENTIAL
PHASE 4
what happens if you STEEPEN the SLOPE of PHASE 4 of the SAN ACTION POTENTIAL
INCREASES HEART RATE
(next action potential comes sooner)
what happens if you FLATTEN the SLOPE of PHASE 4 of the SAN ACTION POTENTIAL
DECREASE HEART RATE
(next action potential comes later)
… TONE STEEPENS the SAN PHASE 4
SYMPATHETIC TONE
(increases heart rate)
…. TONE FLATTENS the SAN PHASE 4
PARASYMPATHETIC
(slows heart rate)
in ECG what does the P WAVE show
ATRIAL DEPOLARISATION
in ECG what does the QRS COMPLEX WAVE show
VENTRICLE DEPOLARISATION
in ECG what does the T WAVE show
VENTRICULAR REPOLARISATION
in PHARMACOLOGY which IONS HOMEOSTASIS are used to treat ABNORMAL HEART RHYTHMS - ANTIARRYTHMICS
SODIUM (eg Flecainide)
CALCIUM (eg Verapamil)
what can also be used that influence Na+ Channels
LOCAL ANEASTHETICS eg Lidocaine
Ca+ Channel blockers can also be used to control..
BLOOD PRESSURE
in ANTIHYPERTENSIVES eg Amlodipine
HIGH SERUM POTASSIUM (HYPERKALAEMIA) has what effect on the HEART
(caused be renal failure or drugs ie ACE inhibitors)e
- SLOWED CONDUCTION
- HEART BLOCK (block in AV node)
LOW SERUM POTASSIUM (HYPOKALAEMIA) has what effect on the HEART
(caused by GI loss, drugs ie diuretics)
INCREASED incidence of TACHYARRHYTHMIAS
- RAPID HEART RHYTHMS