Origin And Conduction Of Cardiac Impulse / Force Generation By The Heart / The Cardiac Cycle Flashcards
Where does the excitation of the heart originate and what is its role?
Sino-atrial (SA) node:
- Cluster of specialised pacemaker cells
- Controls sinus rhythm
- Have no stable resting membrane potential, they generate spontaneous pacemaker potentials
- Spreads excitation via gap junctions to both atria or AV node
Pacemaker potential:
- T-type low voltage channels open
- Funny current causes hyperpolarisation via slow influx of Na+
- Decreased K+ effux, Ca2+ influx
- Depolarisation via opening of long lasting Ca2+ channels causing Ca2+ influx
- Repolarisation via inactivation of Ca2+ channels
- Activation of K+ channels causing K+ effux
AV node:
Only point of electrical contact between atria and ventricles
Delays conduction
Bundle of his and network of purkinje fibres carry impulse from AV node to myocardium
Action potential in myocytes:
Phase 0: Na+ influx
Phase 1: Na+ channels close, K+ effux
Phase 2: Ca2+ influx
Phase 3: Closure of Ca2+ channels, K+ effux
Phase 4: Resting membrane potential reached
Phases 0,3,4: Generation of action potential in pacemaker cells
Phase 2: Allows muscle cells to contract and depolarise, switches on systole
Bradycardia and tachycardia:
Bradycardia: Resting HR below 60
Tachycardia: Resting HR above 100
What is an ECG and what do the leads detect?
Surface electrodes detect waves of depolarisation and repolarisation
Lead 1: Right arm - left arm
Lead 2: Right arm - left leg
Lead 3: Left arm - left leg
ECG waves
P-wave: Arterial depolarisation
QRS complex: Ventricular depolarisation
T-wave: Ventricular repolarisation
PR interval: AV node delay
ST segments: Ventricular systole
TP interval: Diastole
How ANS effects HR
Vagus nerve (parasympathetic):
- Exerts continuous influence on SA node under rest
- Vagal tone: slows intrinsic HR from high HR to normal resting HR
Vagal stimulation (parasympathetic):
- Slows HR from SA node
- Increases AV node delay
- Acetylcholine on M2 receptors
Sympathetic stimulation:
- Increases HR from SA node
- Decreases AV node delay
- Noradrenaline on B1 adrenoreceptors
Cardiac muscle structure:
Striated (due to regular arrangement of contractile protein)
Myocytes coupled by gap junctions
Desmosomes: In intercalated discs, mechanical adhesion between adjacent cells
Myofibrils: Contractile muscles that makes up muscle fibre
Actin - causes lighter appearance
Myocyin - causes darker appearance
Sacomeres - actin and myocyin arranged
Sliding filaments mechanism:
ATP-dependent interaction between sliding actin (thin) and myocyin (thick) filaments
ATP and Ca2+ required
How excitation of cardiac muscle results in contraction:
Ca2+ released from sacroplasmic reticulum (SR), depends on presence of extracellular Ca+
Power up: Myocin hydrolyses ATP before binding
Power stroke: Myocin releases ATP once blinded
Diastolic and Systolic AP:
Diastole:
- Ventricular muscle relaxes
Systole:
- Ventricular muscle contracts
- Ca2+ sourced from Phase 2 of AP
- Causes more Ca2+ release
Importance of a long refractory period:
Prevents generation of tetanic contraction
Plateau phase, Na+ channels are in depolarised closed state
Descending phase: K+ channels open, membrane can’t depolarise
Absolute RP: No stimulus can depolarise cell
Relative RP: Large stimulus can generate AP
Stroke volume:
Volume of blood pumped out by left ventricle per heart beat
SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
EDV = Volume of blood in each ventricle at end of diastole
After load: Resistance when heart is pumping causes extra load imposed after heart contracts
- Heart can’t eject full volume so EDV increases
Intrinsic control of SV
Intrinsic: SV changed due to change in diastolic length / stretch of myocardial fibres
Starlings law (intrinsic): Matches SV of RV and LV
- Low EDV = Weak contraction, low SV
- High EDV = Strong contraction, high SV
Extrinsic control of SV
Via nerves and hormones
Inotropic effect: Stimulation of sympathetic nerves increases force contraction
- Positive: Increased SV
- Negative: Decreased SV
Sympathetic stimulation:
- Increased force of contraction increases Ca2+ influx
- BP and ventricular relation increases
Cardiac cycle definition
All events that occur from the beginning of one heartbeat to the beginning of the next
Different phases of the cardiac cycle
Passive filling
- Atria and ventricles relaxed
- Blood flows into right and left atria and then into ventricles
Atrial contraction
- Atrial depolarisation causes atria to contract, forcing blood into ventricles and completing EDV
Isovolumetric ventricular contraction - systole
- Atrial pressure falls after contraction
- This causes AV valves to close (S1 sound)
- Ventricle depolarisation os halfway through, rapidly building pressure in ventricles
- No blood is ejected, ventricular volume unchanged
Ejection
- Aorta and pulmonary valves open when pressure in ventricles is greater than in aorta/pulmonary trunk
- Blood pumped into aorta and pulmonary artery
- Ventricles relax, decreasing pressure in ventricles
- This causes aortic and pulmonary valves to close (S2 sound)
Isovolumetric relaxation - diastole
- All valves are closed
- Ventricles relax causing AV valves to open
- Ventricles bill with blood and cycle repeats
Changes in ventricular pressure and volume throughout the cardiac cycle
Systole - Ventricular pressure increases
Diastole - Ventricular pressure decreases
Systole - Ventricular volume decreases
Diastole - Ventricular volume increases
Status of the heart valves during different stages of cardiac cycle
Filling phase:
- AV valves open
- Aortic/pulmonary valves closed
Isovolumentric contraction - systole:
- AV valves close (S1 sound)
- Aortic/pulmonary valves closed
Ejection:
- AV valves closed
- Aortic/pulmonary valves open at start then close (S2 sound)
Isovolumetric relaxation - diastole:
- AV valves closed at start then open
- Aortic/pulmonary valves closed
Origin of normal heart sounds S1 and S2
S1 (lub):
- Caused by closure of mitral (left AV) and tricuspid (right AV) valves
- Marks beginning of systole
S2 (dub):
- Caused by closure of aortic and pulmonary valves
- Marks end of systole and beginning of diastole
Mitral location: 5th left intercostal space
Tricuspid location: 4th left intercostal space
How is arterial pressure maintained during ventricular diastole
Ventricles relax, reducing pressure in ventricles which cause AV valves to open
Clinical significance of the estimation of Jugular Venous Pressure (JVP) and outline JVP waveforms
Stretch and recoil of arteries keeps blood moving during diastole despite arterial pressure falling to nearly 0
JVP occurs right after arterial pressure waves
