Download The Heart Functions as a Pump. How do we measure the electrical

The Heart Functions as a Pump. How is the pump
action controlled by regulated waves of cell-cell
depolarization within the pump? 2/10
Review: What are the steps to a cardiac cycle of contraction?
How do the heart valves maintain one-way blood flow in two
separate circulatory loops?
How does the heart work as a pump?
What is the pathway taken by the wave of depolarization in the
heart?
What is the difference between nodal and contractile
depolarization?
What is a pacemaker potential?
How do cells initially become depolarized?
(LEAKAGE=autorhythmicity)
How does the action potential pass between adjacent cells?
(PASSAGE=electrical syncitium)
Your heart pumps blood using a five step Cardiac Cycle:
• Remember the two equal cycles: Pulmonary AND
Systemic
1) Diastolic Filling of Atria and Ventricles (V. Diastole)
– Semilunars are closed and AV valves are open!
2) Atrial Systole (VIP: occurs towards the end of V.
Diastole)
– Ventricles are primed with atrial blood (“topped off”)
– Semilunar valves closed
3) Isovolumetric Ventricular Contraction (V. Systole)
– Semilunar valves remain closed, AV valve flaps are
close by back flow of blood into atria when the
ventricular pressure begins to increase.
– Pressure is generated until
Ventricular mmHg > Arterial mmHg
• 4) Ventricular Ejection (V. Systole)
– When Vent P > Arterial P, semilunars open and blood can
exit the ventricle
– Volume of blood ejected from ventricle is dependent on
magnitude of pressure gradient
– Semilunar valves must open before ejection can begin!
• 5) Isovolumetric Ventricular Relaxation (V. Diastole)
– End of contraction, semilunars close when VentP<
Arterial P
– AV valves open and diastolic filling begins next cycle
• 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
Remember that the AV and semilular valves close to
prevent flow of blood from high to low pressure back into
the atria or ventricles!
Your heart pumps blood using a five step Cardiac Cycle:
• Remember the two equal cycles: Pulmonary AND Systemic
1) Diastolic Filling of Atria and Ventricles (V. Diastole)
2) Atrial Systole (VIP: occurs towards the end of V. Diastole)
3) Isovolumetric Ventricular Contraction (V. Systole)
4) Ventricular Ejection (V. Systole)
5) Isovolumetric Ventricular Relaxation (V. Diastole)
• 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.
How do 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!
VentricularEjection/StrokeVolume(SV): blood leaving vent. (70ml)
– “Ejection Fraction (EF)”
– EF=SV/EDV X 100 = 70ml/130ml X 100 = 54%
– SV can be larger and EF can be up to 90% during exercise!
End Systolic Volume (ESV): Amount left in vent. After systole
– ESV=EDV-SV=130ml-70ml =60 ml (amt. remaining during
isovolumetric relaxation)
– Heart disease= a weak ventricle so the EF is small and ESV
large
Cardiac Output (CO): amount pumped by a ventricle/minute
– CO= SV X HR = 70 ml/beat X 75 beats/min = 5,000 ml/min
– CO=SV X HR = 100 ml/min X 50 beats/min = 5,000 ml/min
– (X2 for “whole heart”: Rt/Lt ventricles pump equal volumes:
5X2=10 L/min)
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.!
Put ECG, Aorta, Ventricle, Atria, BP, heart sounds and pressure
all together to measure cardiac output. If the RR-interval is 1.0
seconds, what is the aortic BP, SV and CO? VIP Diagram
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!
Non-Contractile Cells!
Remember: this is depolarization in single cells, not the whole heart!
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)