9/17c Cardiac Physiology (Biomedical Sciences) Flashcards
• Describe basic anatomy of the major components of the cardiovascular system • Describe the interaction of the electrical and mechanical events in the cardiac cycle • Describe the mechanisms whereby the determinants of the cardiac output are regulated to maintain homeostasis (regulate different temperatures and processes in the bodY) during different levels of metabolic demand Describe how the determinants of cardiac output are evaluated clinically
Functions of the CardioPulm system
- Deliver enough blood to tissues for metabolic demands
- Oxygen to tissues
- maintain homeostasis/temp regulation
- blood carries waste out of tissues
- delivery of hormones
- re-distributes blood flow
How to measure the range of metabolic demand
- measure amount of oxygen our body is utilizing (VO2 max)
- Useful because most of the cellular reactions in the body require oxygen
Metabolic need, SV, HR, CO at different states***
- rest: Metabolic need = 250ml O2/min, HR = 72bpm, SV = 70 ml, CO = 5040 ml/min, 5 l/min
- max exercise: metabolic need = 5,000 ml O2/min, SV = 140ml, CO = 25,200 ml/min, 25 l/min
Quantify output of cardiovascular system using:
Cardiac Output
CO = HR x SV
Volume of blood per unit time
Increases in CO and metabolic demand at different exertion states
- Metabolic Demand increases 20 fold from rest to exertion
- CO increase 5 fold from rest to exertion
what percent of CO goes to skeletal muscle?
15-20% at rest (0.75 l/min)
80-85% during exercise (20 l/min)
20-30 fold increase
RBC Pathway
R atrium > Tricuspid Valve > R ventricle > Pulmonary Artery
Skeletal muscle cell concentration gradients
set up through sodium potassium pumps (K+ out and Na+ in) - ELECTROCHEMICAL GRADIENT
- High concentration K+ INSIDE of the cell
- High concentration Na+ OUTSIDE of the cell
What is the resting membrane potential of a muscle cell?
-90mV
Inside is negative wRt outside
In order to depolarize the membrane, what do we need?**
electrochemical gradient that reaches
Difference between cardiac muscle and skeletal muscle**
1-2 ms for skeletal contraction
300 ms for cardiac contraction
PLATEAU caused by two things opposing one another
1. slow acting calcium channels opening (Ca++ inside is really low) allow calcium to come in and depolarize the membrane
2. K+ exits the cell and hyperpolarizes the membrane (more negatively charged membrane)
Basis for the Electrochemical Signal of the Cardiac Action Potential Cycle
Upstroke - Na+ channels open and depolarize (INWARD)
Plateau - Ca++ channels open (INWARD) and K+ channels open (OUTWARD)
Downstroke - Ca++ channels close and K+ channels stay open to hyperpolarize the membrane (OUTWARD)
Will a de-innervated heart continue to beat on its own?
YES because of cardiac automaticity due to unstable resting membrane potential
- Normal myocytes for force production until depolarization
- Nodal cells of the Conducting pathway generates depolarization that leads to AP
what causes automaticity/unstable resting membrane potential of nodal cells?**
- Inward current of Na+ (not as much as myocytes)
- Calcium channel gradual opening
- Funny current that is gradually inward positive charge
- when membrane potential reaches threshold, there is an action potential
Rapid Conducting pathway of the heart***
allows wave of depolarization to move through the heart in an organized way
- SA Node contracts atria (depolarization of atria) while ventricles are relaxed
- AV Node gets the wave of depol and causes coordinated push to move blood from atria to ventricles, slows down conduction of the impulse and allows for ventricular filling to be maximized
- Bundle of His
- Bundle Branches
- Purkinje Fibers
Why does the SA node drive HR?
Intrinsic rates to reach threshold
- SA node has the highest intrinsic rate (60-100bpm)
- AV node and bundle of his have intrinsic rates too, but they are not as fast and they won’t be able to fire during the refractory period
Refractory period
after AP, period of time before which we can’t refire an AP
Overdrive suppression***
high intrinsic rate of the SA node makes it the dominant pacemaker
Pathological conditions that have other sources of depolarization of the heart
ectopic foci
-not in the normal place
How do you evaluate the signal of the heart?
ECG
- P wave, atrial depolarization electrical signal (lines up with AP generated in SA node and spread in atrial muscle)
- Pause, AP conducted through AV node
- QRS, ventricular depol transmission of ap through bundle of his, bundle branches, purkinje fibers and ventricular muscle.
- plateau
- t-wave, vent repolarization back to baseline
Atrial repol in QRS complex
Normal sinus rhythm
- Space between r waves is consistent
- Rate is between 60-100bpm *intrinsic rate for SA node
- Normal Shape
Vent Systole on the ECG
beginning of QRS to the end of t wave
Vent Diastole in ECG
end of t wave to beginning of next qrs
what can go wrong with heart rhythms/rates?
Sinus tachycardia (close p waves) Sinus bradycardia (farther p waves) Premature ventricular filling (different shape, wide and bizarre signals - ectopic foci) ventricular fibrillation (wavy line) atrial fibrillation (no defined p-wave)
EC coupling/signal producing a heart beat
Excitation contraction coupling
-mechanism in skeletal muscle is different from cardiac
SYSTOLE
-influx of Ca++ during AP causes ryr receptor on the SR to open and release calcium = Calcium induced, calcium released
-Ca++ interacts with myofilaments – it binds to troponin, causes it to shift and allows myosin and actin to interact and contract
DIASTOLE
-myosin actin relationship will continue as long as Ca++ levels in the cell are elevated
-Ca++ Falls as it is transported:
–into SR via SERCA pump
–out of cell by membrane Ca++ pump and Na-Ca exchanger
-Fall in Ca++ causes troponin to shift, blocking actin/myosin
why do we need mechanisms for rapid contraction and rapid relaxation?
so the ventricles can refill with blood and relax
ATPase
breaks down ATP
Relaxation/diastole
- relaxation is when Ca++ are pulled out of sarcoplasm and back into SR or outside of the cell with the SRCA pump (requires ATP)
- Na+/Ca++ Exchanger that pumps intracellular Ca++ outside of the cell
what controls strength of beat and relaxation of the heart?
Calcium!
How do we evaluate the mechanical response of the heart?
echocardiography
- Stroke volume = EDV - ESV
- Ejection fraction = SV/EDV
End Diastolic Volume
Largest volume in the heart
End Systolic Volume
Smallest volume in the heart
What can go wrong with the beat of the heart?
- Valve disease, stenosis and regurgitation
- Decreased Contractility and Relaxation
- -Systolic dysfunction (decreased contractility)
- -Diastolic dysfunction (decreased relaxation)
Cardiac Cycle (mechanical steps)
- Systole
- Isovolumetric Contraction
- Ejection - Diastole
- Isovolumetric Relaxation
- Passive Filling of Ventricle
- Active Filling of Ventricle (Atrial systole or atrial kick)
Wigger diagram
Left ventricular pressure and time
Left ventricilar pressure
starts in diastole where pressure is low, but pressure is increasing because we are filling the chambers with blood
-atria contract and there is a slight decline that lines up with the first heart sound - where mitral valve closes
what causes valves to open/close?
pressure gradient between the chambers
Mitral valve
- on the left side, between the atria and the ventricle
- during diastole, mitral valve is open and allows blood flow from atria to ventricles
- Closes when there is an increase in pressure in the ventricle (depolarization of ventricle)
closure of mitral valve is what?
mechanical indication of the beginning of systole
during systole, where does blood go?
out of LV and into the aorta through the aortic/semilunar valve
During diastole, where does the blood go?
into the ventricle from atria
isovolmetric contraction phase
building pressure until the pressure in the LV is greater than the aortic pressure and starts to push open the aortic valve
Ejection
aortic valve opens and blood begins to eject
isovolumetric relaxation
left ventricle begins to relax as blood is moving into aorta, until LV pressure dips below aortic pressure
When ventricular pressure continues to dip below aortic pressure then below atrial pressure what happens?
- Aortic valve closes
- Mitral valve opens because we are back in diastole
- -rapid inflow, period where blood rushes into left vent
- -middle phase, diastasis
- -atria contract, then the cycle begins again
Closure of the aortic valve
mechanical marker of the end of systole
second heart sound (DUB)
Heart sounds are:
- closure of mitral valve - lub
- closure of aortic valve - dub
time between lub and dub is systole
time between dub and next lub is diastole
How is HR regulated?
-in a time vs mV graph, we see the membrane potential of the nodal tissue
-the line reaches threshold and we get an AP
-the slope of the line needs to be manipulated to change the HR
DONE THROUGH ANS
Sympathetic NS
- +Chronotropic (chrono = time, tropic = changes) effect increase HR. SAnode, AV node and ventricles are innervated with receptors for SNS.
- Norepi is the neurotransmitter released by SNS nerves and act on Beta1 receptors in sinoatrial node to increase HR
- Play around with Na and Ca channels that are responsible for funny current that causes unstable resting membrane potential
Parasympathetic NS
- -Chronotropic Effect
- Ach is released from vagus nerve that acts on muscarinic receptors on nodal cells to decrease HR
- Plays around with Na and Ca+ channels that are responsible for funny current and decreases slope of resting membrane potential
Does an increase in HR ALONE increase CO?
Increasing HR alone is NOT sufficient, because the amount of time available for diastole shrinks, so ventricular filling time is not enough
when HR is above 150, the time is so short that we compromise filling
When exercising or stressing to the point where your HR goes above 150, why does your CO not go down and go up instead?
enhanced venous return!
Overall, greater venous return
1. veins have receptors on them that are responsive for SNS neurotransmitters (norepi and epi), when SNS is activated it causes the veins to constrict and it augments venous return
2. Muscle pump - everytime muscles contract, they squeeze veins embedded in them and helps to push blood flow back to the heart
Are veins a reservoir of blood in the absence of venoconstriction?
YES
factors that influences of SV
- preload - degree of stretch on myocardial cells and volume of blood in the ventricles at the end of diastole (EDV is the index of preload)
- -Larger the preload, the higher the SV (direct relationship) - Contractility - strength of the contraction; Ca++ Dependent
- -Larger the contractility, the higher the SV (direct relationship) - Afterload - load that the ventricle has to overcome in order to eject blood.
- -Larger the afterload, the smaller the SV (indirect relationship)
how much pressure does the left ventricle have to generate in order to eject blood?
More than the pressure in the aorta
Mean articular pressure is the same as
aortic pressure
Preload broken down
- Vent EDV is 3D rep of length, SV is analog to tension (length/tension relationship curve)
- proportional to the degree of stretch on the myocyte/myocardium.
- SV with higher EDV causes increased stretch on myocyte, causes a stronger contraction, and generates a GREATER SV
Active length tension curve, NOT passive length tension curve (generally)
- frank starling curve//length/tension relationship proportional with PRELOAD
- –short muscle can’t create force
- –lengthen muscle there is better overlap between cross bridges
- –lengthen too much and no longer get overlap between cross bridges
What affects preload?
- venous return (receptors for epi and NE; muscle pump)
- duration of diastole
Afterload broken down
- Load ventricle has to overcome to eject blood
- index is aortic pressure
- higher the aortic pressure, hard to eject blood, SV decreases
- increase in afterload is escalade (less displacement b/c higher force necessary)
- decrease in afterload is smart car (more displacement b/c less force necessary)
What affects afterload?
- Increase aortic pressure and therefore afterload
1. hypertension
2. aortic stenosis - Decrease aortic pressure and therefore afterload
1. hypotension
What affects contractility?
- Calcium dependent strength of the beat
- (+)ionotropic affect > increase intracellular Ca++ > stronger contraction > greater stroke volume
- (-)ionotropic affect >decrease intracellular Ca++ > weaker contraction > smaller SV
What causes a +ionotropic affect?
- Physiological - SNS>NorEPI acts on Beta1 receptors to increase intracellular Ca++
- Pharma - cardiac glycosides > Increase intracellular Ca++
what causes (-) ionotropic affect?
- hard to do with SNS, but PNS doesn’t have much to do with contractility b/c not many muscarinic receptors
- Drugs that are calcium channel blockers (beta 1 blockers) to decrease intracellular Ca++
