G1 + G2 electric and anatomy Flashcards
Give 5 differences anatomically between the RV and LV
Functionally what are the main differences between RV and LV 5
Draw how an RV and LV pressure volume curve looks Different
What feature of the ANS is unique with respect to the heart?
The only site where PSNS tone is tonically active at the SA node instead of the SNS being the tonically active agent
What receptors does acetycholine interact with at the SA node
M2
- Speed of conduction through specialised Purkinje fibres
1-4m/sec
AP duration in ventricular cells
- Action potentials lasting 300msec in ventricular cells
Phase 4 of the myocardial action potential - features 2
- Stable Resting membrane potential = -85 to -95mV
- Maintained by I (kI) inward rectifying potassium current balancing the sodium and calcium entering the cell leading to equal inward and outward current
At what point is the depolarisation thewshold reached in cardiac muscle cells
-65mV
How fast is depolarisation in cardiac myocytes? In seconds and in V/sec
By how much amplitude?
What triggers to do so?
What electrolytes move
- Na channels opening at -65mV voltage gated
- Rapid depolarisation over 1-5 10 thousands of a second through fast voltage gated sodium channels increasing sodium permeability and entrance into the cell
- Simultaneous reduction in potassium conductance (potassium leaving cell) - iK1
- Depolarisation by 105mV - high amplitude
- VMax 200-800 V/sec
Describe phase 0 of the cardiac action potential
- Na channels opening at -65mV voltage gated
- Rapid depolarisation over 1-5 10 thousands of a second through fast voltage gated sodium channels increasing sodium permeability and entrance into the cell
- Simultaneous reduction in potassium conductance (potassium leaving cell) - iK1
- Depolarisation by 105mV - high amplitude
- VMax 200-800 V/sec
Phase 1 of the cardiac action potential
- Rapid repolarisation through voltage sensitive transient outward potassium currents (I to) triggered through voltage changes and decreases in sodium permeability (inactivation of fast sodium channels)
- Drop in membrane potential to 0-10mV relative to intercellular fluid
Phase 2 of the cardac action potential features 3
- Prolonged plateau ~0mV
- Lasting 100-200msec
- Mediated by L type calcium channels with calcium inflow, and simultaneous potassium outflow balancing electrical potentials
Phase 3 of the cardiac action potential
- Rapid repolarisation through closure of L type calcium channels and potassium efflux through delayed rectifier K current (I kr), I (ks) and I(k1) potassium currents- resting membrane potential again reached at the end of phase 3 as the membrane potential is closer to the equilibrium potential of K
- Refractory periods
◦ Absolute 200msec
◦ Relative 50msec
How long are the 2 main refractory periods
- Rapid repolarisation through closure of L type calcium channels and potassium efflux through delayed rectifier K current (I kr), I (ks) and I(k1) potassium currents- resting membrane potential again reached at the end of phase 3 as the membrane potential is closer to the equilibrium potential of K
- Refractory periods
◦ Absolute 200msec
◦ Relative 5mm sec
Relate action potential and tension
Phase 0 of the action potential relates to what 2
- Phase 0 —> beginning of the Q wave and QRS complex
◦ Initially corresponding to beginning of systole and isovolumetric contraction
Phase 1 and 2 correspond to what part fo the ECG and cardiac cycle
- Phase 1/2 correspond to the QRS + ST interval
◦ Corresponds to systole
◦ Phase 1 - isovolumetric contraction
Phase 3 corresponds to what in the cardiac cycle and ECG
- Phase 3 corresponds to the T wave and repolarisation
◦ Corresponds to the very last period of systole, isovolumetric relaxation and the beginning of diastole
Phase 4 corresponds tow aht in the cardiac cycle and ECG
Diastole
Draw a cardiac action potential for a ventricular myocyte
Draw a cardiac action potential for a pacemaker cell
Compare the speed of response and speed of action potential between a myocyte and pacemaker
Comapre membrane permeability, RMP,. threhsold potential and duration fo action potential between a pacemaker and a myocyte
Compare phases of the action potential between pacemaker and myocyte
How do pacemaker cells depolarise
unstable slow depolarisation due to ‘funny’ current with hyperpolarisation activated cyclic nucleotide gated channels increasing Na permeability of the cell (i.e. cAMP gated allowing autonomic control)
How is ventricular myocyte-myocyte conduction allowed
Gap junctions at intercalated discs
Describe the pathway of normal sinus node activation to depolarisation
◦ SA node —> rest of atria and internodal tracts
◦ Internodal tracts - modified myocytes along atrial wall in parallel with high velocity conduction including through Bachman bundle to the LA
◦ From atria depolarisation spreads to the AV node
‣ Septal part of right atrial base
‣ Responsible for introducing delay between atrial and ventricular systole
‣ Slow conduction - 0.05m/s
‣ The only pathway from atria to ventricle
◦ Bundle of His and His-Purkinje system
‣ High velocity conduction spreading to ventricular muscle
◦ Ventricular muscle - fast conduction from endocardium outwards to epicardium
◦ SA node —> atrial muscle (RA —> LA) —> AV node (slower conduction) —> Bundle of His —> RIght and Left Ventricular bundle branches —> Purkinje fibres and ventricular muscle cells
Why is there a prolonged refractory period in cardiac muscle?
- Contraction lasts hardly longer than the action potential and throughout this period the cell is in the absolute refractory period - thus it is impossible to summate contractions or tetanus cardiac muscle
◦ Absolute refractory period 200ms
‣ Long absolute refractory period int he AV node prevents retrograde conduction and limits conducted rate to a maximum of ~220
‣ His-Purkinje system also has a long absolute refractory period preventing depolarisation however relative refractory period permits early afterdepolarisation —> this is the reason for refractory period of ventricular myocytes after a VEB
◦ Relative refractory period 50ms
◦ This is due to
‣ Voltage gated channels being inactivated until repolarisation to <-40mV in automaticity fibres and <-60mV in atrial and ventricular muscle
What is the p wave in the cardiac cycle
- SA node firing leading to propogation of atrial depolarisation and subsequent Atrial contraction as the last phase of diastole
◦ SA node firing corresponds to just prior to the beginning of the P wave
◦ Contraction fo the RA occurs midway through the P wave, and LA contraction occurs at the end of the P wave and continues through the PR interval
What is the PR interval and how might it be prolonged
What are the cardiac cycle events relating to the PR interval
- A combination of residual atrial depolarisation and subsequent transition through the AV node adn bundle of His
- AV nodal delay accounts for most of this time period allowing for completion of atrial contraction prior to ventricular contraction to maximise EDV
- The PR interval is the final phase of diastole
- This time may be prolonged by drugs due to
◦ Beta blockers - increase the refractory period fo the AV node by decreasing sympathetic stimulus and calcium permeability during the phase 4
◦ Digoxin - Increased refractory period of the AV node probably by increased vagal activity
QRS complex correlates with what int he ECG and cardiac cycle
How can this be prolonged
- R wave peak represents the initial phase of systole, as isovolumetric contraction begins
- AV valves close
- Atrial relaxation
- This period may be prolonged by drugs due to
◦ Flecainide, lignocaine, Phenytoin, TCAs all block fast voltage gated sodium channels slowing phase 0 with diminished magnitude prolonging the QRS
St interval is what in the cardiac cycle
- Ventricular ejection with semi linear valves opening corresponding the to the rapid ejection early phase of systole
- Rapid atrial filling as the AV valves are pulled downwards enlarging atrial volume
How may the QT interval be prolonged
- The QT interval may be prolonged by the action of drugs bye
◦ Amiodarone and sotalol both prolong phase 3 of cardiac action potential (repolarisation) by acting at potassium channels as antagonists slowing repolarisation and prolonging the absolute refractory period and prolonging the QT interval
◦ Antipsychotics - chlorpromazine/haloperidol, droperidol, quetiapine, olanzapine -block IKr
◦ Type 1A antiarrhtyhmics -procainamide - and it’s metabolite do affect IKr
◦ Type 1C antiarrhtyhmics - flecainide
◦ TCA - amitryptiline - sodium channel blockade
◦ Antidepressants - escitalopram, citalopram, venlafaxine, bupropion, moclobemide - IKr
◦ Antihistamines - loratidine - IKr
◦ Macrolidies and hydroxychloroquine - block rapidcomponent of IKr on delayed rectifier potassium current but also inhibition of metabolism of any of the above agents
What is the T wave - what does it correspond to in the cardiac cycle and ECG
- Represents the beginning of repolarisation and the first phase of the T wave prior to the peak corresponds to late systolic ejection with decreasing rate of ejection as ventricular muscle begins relaxing but semi lunar valves remain open
- At peak of T wave semilunar valves close
- 2nd half fo the T wave represents isovolumetric relaxation
Draw a diagram relating the cardiac cycle to pressures to ECG, heart sounds and ventricular volume
How does the heart anatomically change with aging? 4
‣ LV hypertrophy - in the absence of hypertension, hypertrophy of individual myocytes despite 30% reduction in number of myocytes
‣ Cardiac shape
* Interventricular septal hypetrophy - proximally
* LVOT narrowing - rightward shift of ascending aorta narrowing LVOT tract along with interventricular septal hypertrophy
‣ Valvular sclerosis - stiffening, scarring and calcification - 80% of older people have sclerosis - mucoid degeneration of collagen in valve
‣ Degeneration of sympethetic innervation - axonal degeneration
How does the LV shape change with aging (2)
‣ LV hypertrophy - in the absence of hypertension, hypertrophy of individual myocytes despite 30% reduction in number of myocytes
‣ Cardiac shape
* Interventricular septal hypetrophy - proximally
* LVOT narrowing - rightward shift of ascending aorta narrowing LVOT tract along with interventricular septal hypertrophy
‣ Valvular sclerosis - stiffening, scarring and calcification - 80% of older people have sclerosis - mucoid degeneration of collagen in valve
‣ Degeneration of sympethetic innervation - axonal degeneration
How do the blood vessels change with age
‣ Dilation of aorta and large arteries - aortic root especially by 1mm for every 10 years after 16
‣ Thickening of arterial walls - larger kumen, and thicker wall due to thicker tunica intima and media
‣ Decreased windkessel effect - loss of elasticitiy - high rpessure transmitter to more distal vessels
How does myocardial cell performance change with age?
- Systolic functions
- Increased systolic function in men, stable in women. SV the same, EF the same
- Cardiac output may decrease by 1% per year - HR - decreased maximal HR due to reduced Beta recetor, SA node atrophy, conduction tissue loss, AP prolongation
- Diastolic functions - decreased compliance common with age, increased dependence on atrial kick
- Ability to respond to change - blunted barorecepotr response
- Oxygen demand/work - increased cardiac workload (afterload)
How does the conduction system in the heart change with age
- Decreased maximal HR
- ‣ SA node atrophy - only 10% of SA node cells remain at 70, apoptosis - affects other areas of the condution system also
- Conductive tissue loss
- Action potential prolongation - L type calcium channels deactivate more reluctantly more calcium remains in the cell for longer
How is the vasculature changed with age
- Decreased compliance - glycosaminoglycin in extracellular matrix and thicker walls resulting in higher afterload, wider pulse pressure
- Decreased vasodilatory function with higher resting vessel tone
How do neurohormonal factors change with aging in the heart
‣ Increased ANP secretion - end organ sensitivity decreased though
‣ Increased circulating catecholamine levels - decreased catecholamine receptor sensitivity
‣ Decreased renin, angiotensin and aldosterone concentrations - fall in renin actiivty
Describe the veinous drinaage of the heart
Great cardiac vein (anterior interventricular vein) – the largest tributary of the coronary sinus. It originates at the apex of the heart and ascends in the anterior interventricular groove. It then curves to the left and continues onto the posterior surface of the heart. Here, it gradually enlarges to form the coronary sinus.
Small cardiac vein – located on the anterior surface of the heart, in a groove between the right atrium and right ventricle. It travels within this groove onto the posterior surface of the heart, where it empties into the coronary sinus.
Middle cardiac vein (posterior interventricular vein) – begins at the apex of the heart and ascends in the posterior interventricular groove to empty into the coronary sinus.
Posterior cardiac vein – located on the posterior surface of the left ventricle. It lies to the left of the middle cardiac vein and empties into the coronary sinus.
