Physiology Heart Flashcards
what is the basic structure of the cardiac muscle cells ?
1-one nucleus
2-striated
3-Branched
Path of cardiac impulse through myocardium
1) SAN
2) AVN
3) PURKYNE LECTURE
4) BEAT OF HEART
what is the non-pacemaker action potential? 5 phases (5) why does it look like that? (2)
phase 0=Na+ channels open and na+ floods in. The closing gate is very slow so Na+ concentration rises to +20mv before it closes
Phase 1=SPIKE=closure of Na+ channel gate!K+ channels open = K+ leaves cell so AP is closer to 0 .CL-channels also open = more negative cell and the voltage starts to decline, become more negative (partial depolarisation)
Phase2=slow decline=slow plateaux phase =slow prolonged opening of Ca2+ channels =long plateaux! Ca2+ enter the cell making the cell positive for longer, hence plateaux and K+ is still moving out of the cell!(balancing each other out )
Phase3=2k+ channels = Inwardly rectifying and delayed rectifying. The Ikr channel (inwards rectifying) =allows K+ back into the cell making it positive! However, it CHANGES POLARITY HALFWAY THROUGH PHASE 3=pushes K+ out of the cell (making cell more negative).Ca2+ channels CLOSE
Phase 4=resting membrane potential reached (pacemaker depolarisation phase= na+/ca2+ moves out an k+ going in = sodium potassium pump)
there is a long AP plateaux because the AP lasts around 350 ms = this means no summation of contractions can occur. Summation would mean the heart would have continuous contractions = less time for filling and pump failure ( heart failure )
what is the pacemake cells action potential ?
5 phases
(5)
Phase 0 =Long lasting ca2+ channels open at -40mv =ca2+ enters cell =very positive =graph is rising =depolarisation.
Phase1=absent
Phase2=Absent
Phase 3=K+ channels open allowing K+ out of the cell making it more negative =repolarisation to -60mv
Phase 4= creep potential -40mv depolarisation again =slow rise of ca2+ inside the cell,K+ permeability is reduced (less k+ can leave the cell) so the cell becomes + =creep potential
sodium channels = allow more na+ in than K+ out hence positive charge is maintained.
why is the refractory period important
3
The refractory period of the heart is very long in non pacemaker cells = this is important so that the heart keeps beating!
If the refractory period was short = this would allow summation and hence contraction would occur for a long period of time ! This means the heart would just be contacted and NOT pump = Heart Attack !
it would also not fill properly and cause heart failure!
long refractory period =allows heart to fill
why can’t cardiac myocytes produce a wide range of contractions ? (1)
- because they’re all fused together = SYNCITIUM
- what happens to one , happens to all of them !
what are the events of the cardiac cycle ?
diastole = filling of blood
systole=contraction
remember blood always flows from ….
(6)
Remember blood always flows from HIGH pressure to LOW
Phase 1= Atrial systole=P wave
Phase 2=isovolemic contraction (ventricles contract so pressure increases but VOLUME remains the same )AV valves are closed / semi lunar valves are closed=RS waves
Phase 3=Ventricular systole starts when pressure in Ventricles is higher than that of the aorta /pulmonary artery= semi lunar valves open (S-T WAVE)
Phase 4=Slowing down =Reduced ejection=T wave= pressure in ventricles drop . Semilunar valves close when Ventricular pressure is lower than aortic pressure = END OF VENTRICULAR SYSTOLE AND START OF DIASTOLE
Phase 5= Isovolemic (ventricles relax with all valves closed-volume remains the same) pressure drops rapidly. Atria =Volume increases , pressure drops .
Phase 6=Ventricular Filling starts (diastole) when pressure in ventricles drops bellow atrial pressure ! AV valves open and allow blood to flow from High pressure to low !
p waves ?
QRS complex?
T wave ?
1) P wave =atrial systole
2) QRS=Ventricular systole
3) T wave =disastole
normal cardiac cycle time ?
1=o.8 seconds
2=
p waves ?
QRS complex?
T wave ?
1) P wave =atrial systole =atrial depolarisation
2) QRS=Ventricular systole=depolarisation
3) T wave =diastole=ventricular repolarisation
normal action potential time in skeletal muscles?
normal action potential time in cardiac muscles ?
time for cardiac cycle to complete (atrial systole , ventricular systole , diastole) ?
(3)
1=skeletal muscle AP=2-5ms
2=Cardiac muscle =200-400ms (very long refractory period)
3=one cardiac cycle is around 0.8 sec long !
what is cardiac output and what factors effect it?
CO=SV X HR
stoke volume =volume of blood in ventricles eject (EDV-ESV)normally around 70ml/beat
what factors affect cardiac output?
positive chronotopic factors and negative chronotopic factors? ( increase and decrease HR)
think about the CO …
CO=HR X SV HR: \+ sympathetic nervous system = adrenaline and noradrenaline \+thyroid hormones (T3/T4) \+Body temperature \+increases CA2+ levels \+peripheral chemoreceptors -too much k+ SLOWS DOWN HR -parasympathetic release of ACH (acts on muscarinic recptor ) decreases heart rate
SV: 1)PRELOAD (EDV-ESV) -more stretch leads to more preload -increased venous return 2)CONTRACTILITY: \+ ca2+ =increase contractility \+/-drugs -thyroid hormones -inhibitors include : Beta-blockers ,ca2+ blockers -high k+ decreases contraction -acidosis causes a decrease in contractility -increase na+ decreases contractility
3)AFTERLOAD (Resistance which has to be overcome to pump blood into artery )
-faulty valves can increase afterload by increasing resistance
-vasoconstriction of arterioles and venues =pressure backs up into the aorta
-
how can you alter heart rate ?
7
HR:
+ sympathetic nervous system = adrenaline and noradrenaline
+thyroid hormones (T3/T4)
+Body temperature
+increases CA2+ levels
+peripheral chemoreceptors
-too much k+ SLOWS DOWN HR (decreases contractility )
-parasympathetic release of ACH (acts on muscarinic recptor ) decreases heart rate
how can you alter stroke volume ?
what are the 3 factors which affect SV?
(10)
SV:
1) PRE LOAD (EDV-ESV)
- more stretch leads to more preload
- increased venous return (muscular milking ,respiratory pump (pressure in thoracic cavity, abdominal cavity sucks blood from Ab–>thoracic cavity (high pressure to low ))
2) CONTRACTILITY:
- ca2+ =increase contractility
- drugs
- thyroid hormones
- inhibitors include : Beta blockers ,ca2+ blockers
- high k+ decreases contraction
- acidosis causes decrease in contractility
- increase na+ decreases contractility
3) AFTERLOAD (Resistance which has to be overcome to pump blood into artery )
- faulty valves can increase afterload by increasing resistance
- vasoconstriction of arterioles and venues =pressure backs up into the aorta
