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
