Remember the two ventricles BOTH do these activities at about same time with the same volumes at two different pressures!
While “Atrial” Systole does occur, it is not as clinically important because the atria only do about 5% of the work done by the ventricles, so they just don’t use as much ATP or need as much oxygen.
Remember that the AV and semilular valves close to prevent flow of blood from high to low pressure back into the atria or ventricles!
How does pressures change in the heart chambers and arteries during the cardiac cycle when you are healthy? Memorize List!
Units of Pressure: measured in mmHg is the ability of fluid pressure to maintain a column of mercury. Yes it’s archaic but it’s the unit used!
Pressure gradients let blood move! ↑ gradient:↑movement point A B
Atrial Pressures : Simply create enough P to load blood into ventricle
-Right Atrium: 0-10 mmHg and the Left Atrium: 0-10 mmHg
Ventricles: MUST generate enough pressure to load blood into arteries
Right Ventricle: 0 to ~ 15-25 mmHg
Left Ventricle: 0 to ~ 120mmHg
If pressure in ventricle is not great enough No Blood Exits Ventricle
Arterial Pressures : Systolic pressure is from Vent Systole and Diastolic is pressure just before next loading from ventricle (Contraction).
-Always expressed: Systolic mmHg/Diastolic mmHg
-Pulmonary Artery: 15-25/8 tough to “feel” ( a very short circuit )
-Aorta: 120/80 felt as a “Pulse” (a long-high resistance circuit)
Venous Pressures: always very very low (sometimes even negative )!
-VenaCava and Pulmonary Veins: 5/0 or lower ( WHEN HEALTHY !)
The volume of blood pumped by a ventricle per minute is the cardiac output of that ventricle! How is CO calculated? Memorize!
How do we get the ventricle ready to push blood out?
Most ventricular filling passively occurs as blood drains from vena cava and pulmonary veins through atria and into the apex (down hill) by simple gravity and draining…..water pours out of a glass onto the floor by the same effect.
End Diastolic Volume(EDV): ml of blood in ventricle after the “kick” Pre-systole (130 ml)
Mostly from passive filling during Vent and Atrial diastole, plus a small bonus from atrial systole (about 100 ml + 30 ml from kick)
Isovolumetric Contraction : no volume change (hopefully)
AV Valves just closed and Semilunars are not yet able to open!
Volume in ventricle does not change but pressure on this 130 ml goes up until pressure in ventricle is greater than in the artery in the blood on other side of the semilunar valve!
Range (cardiac reserve): CO can get up to 35 L/min/Ventricle for Olympic Athletes! Your Blood volume (4-7 L) must be recycled many times/min at 35 L/min
Will I need to do the math for the calculation we just looked at on a lab or lecture test? Answer: Yes Will I get to use a calculator: No Will math be “easy”: Yes
Formulas should be understood for what they are…. a logical prediction of what the body does.
Know basic formulas we just looked at.
Know normal values we just looked at.
Know how to calculate missing information given a set of known facts.
KNOW HOW AND WHY WE MODIFY C.O.!
SA Node-->(Atrial depolarization/contraction) AV Node Bundle of His Lt/Rt Bundle Branch Pukinje Myocardium (Depol./Contract)
How do depolarizations pass between cardiac cells?
Intercalated discs hold adjacent cardiac cells together and the gap junctions create tiny pores in the discs between the cells allowing passage of ions like Na+ and Ca++, this unites all cardiac cells into an electrical syncitium (all connected).
Conduction Path: SA Node Atria AV Node Common bundle branch Bundle of His R/L Bundle Branches Purkinje fibers Myocardium (contractile cells here).
Note: the Conduction rates and Consequence of rates in different locations in the pathway are not the same…this is very important!
Then the wave of depolarization (excitation) spreads from endocardium to epicardium (Inside to Outside)
V.I.P. Atrioventricular septum is normally non-conductive to depolarization! Depol only passes through the AV-Node!
V.I.P. There is a bit of contraction in the interventricular septum prior to the walls of the ventricles (this is clinically significant!)
Heart Rhythm: is the heart conduction coordinated?
Nodal vs. Arrhythmia vs. Ectopic Foci vs. Fibrillation
ACTION POTENTIAL IN INDIVIDUAL CELLS vs. DEPOLARIZATION OF ENTIRE HEART (MANY CELLS CONNECTED BY GAP JUNCTIONS) .
HUGE Functional Difference : Pacemaker Cell vs. Contractile Cell
SA NodalCell(AV nodal or conduction)=(no contractile force)
Cardiac Myocyte (force generation=contractile)
Speed of Na+ leak determines rate of depolarization for SA/AV-Nodes Very Steep Depolarizes Fast Rapid Heart Rate
Not Steep: Cells depolarize slowly take more time to reach threshold for voltage gated Na+ channels to open Slow Heart Rate
Absolute refractory period determines rate of depolarization by determining time the cell must wait until it can be depolarized again
Myocytes and Timing: Why a delay in the onset of contraction ?
Na+ channels must open and let Na+ into cell
Ca++ gets inside myocytes
Ca++ must find troponin and pull it off actin
Actin must find/bind myosin
Actin must ratchet across myosin and generate force
Ca++ Slow to exit myocytes
These all add to the x-axis (time) of contraction
This generates force in ventricle: Isovolumetic Contraction Ejection
SA Nodal cells are non-contractile and rhythmically depolarize themselves and adjacent cells. Nodal cells eventually depolarize adjacent contractile cells via gap junctions. As a result, the depolarizations of contractile and non-contractile cells are very different! Remember: this is depolarization in single cells, not the whole heart! Non-Contractile Cells!
Agents like epinephrine speed up the heart rate and the parasympathetic NS (ACH) slows the heart down. What happens to the rate of membrane leakage (pacemaker potential) to accomplish this change in heart rate at the SA Node? Before and after Sympathetic Stimulation +pacemaker potential Longer period between depol Shorter period between depol Longer time to next depolarization Stimulation of the parasympathetic NS slows down the heart rate by hyperpolarizing the SA node and decreasing its leakiness (pacemaker potential)