normal sinus rhythm:
normal heart rate of ~70 bpm
abnormal heart rate
: slow rate of <60 bpm *Could be normal for someone with a very strong heart, like an endurance athleteeach beat pumps more
: fast rate of >100 bpm *May be experienced in a healthy way during physical activity
sick sinus syndrome:
problem with SA Node, causes abnormal heart rhythm
: can develop in the heart, causing extra contractions (extra-systoles)
extra contractions of the heart result of ectopic pace maker
occurs when there is a transient unidirectional block in the heart, causing the impulse to keep going around and around instead of stopping
: heart can still beat in synchrony up to 200-350 bpm but the heart is not as effective at circulating blood - causes shortening of ventricular diastole so that the heart tissue doesn't get enough oxygenated blood from the pulmonary veins
when electrical impulse doesn't stop and start, but keeps going - circus rhythm - causes heart to stay contracted so that blood flow stops
stopping the action potential in order to throw all of the cardiac muscles into a refractory period so that they can resume contractions at normal sinus rhythm
amount of blood pumped out by ventricles per heart beat
amount of blood left in ventricles at end of ventricular diastole
: stroke volume times heart rate
contractility (force of contraction):
One of the extrinsic controls over cardiac output. For atria, symp ns input causes increase in force and parasymp ns input causes decrease in force. Ventricles contractility only affected by symp ns increase in symp input causes increase in force of ventricular contractions. *Frank Starling Law of the Heart
: One of the intrinsic controls over cardiac output volume of blood that provides force in ventricles Frank Starling Law of the Heart *End diastolic volume affects preload
One of the intrinsic controls over cardiac output the force that the heart has to overcome to get blood out into circulatory system directly related to resistance to blood flow *vessel radius
to blood flow in circulatory system is controlled by vessel radius and affects the afterload in the heart and therefore the cardiac output
: vol. of blood out of each ventricle per minute affected by contractility, preload, afterload, and heart rate
: any drop in cardiac output for any reason
myocardial infarction is a heart attack
: chest pain due to ischemia (insufficient blood flow for organ to function) can be due to incomplete blockage, has to do with a reduction in blood flow to the heart *causes symptoms similar to a heart attack but not as severe
build up of plaque in the arteries, causing "hardening" of the arteries
: blood clot
travelling blood clot
2. You should be able to explain what is meant by "passive" ventricular filling
Most of the blood enters the ventricles passively from the atria. Only a small portion of the blood is actually pumped from the atria to the ventricles by the contraction of the atria.
1 degree heart block:
PR interval > 0.2s It is longer then normal ( PR interval is the time the impulse takes to move from the Atria to the Ventricle.)
2 degree heart block:
: not all of the impulses from the SA Node are making it to the AV Node
3 degree heart block:
: none of the impulses from the SA Node are making it to the AV Node
You should be able to explain the cardiac cycle.
When heart is completely relaxed (diastole), the AV valves are open and blood enters the ventricles passively from the atria. Then the atria contract (atrial systole) while the AV valves are open and more blood is pumped from the atria to the ventricles. Next the pressure from the blood in the ventricles causes the AV valves to close. The ventricles contract (ventricular systole), the semilunar valves open, and blood is pumped out of the ventricles into the aorta and pulmonary arteries. Once the pressure in the aorta and pulmonary arteries reach a certain level, the semilunar valves shut and the heart relaxes again (diastole).
5. You should be able to explain why when heart rate becomes too high, cardiac efficiency decreases.
When the heart rate becomes too high, the ventricles cannot keep up with the atrial contractions and they do not spend enough time in diastole for the myocardia to become sufficiently oxygenated.
6. You should be able to explain the relationship between cardiac output, stroke volume, and heart rate.
Cardiac output is equal to stroke volume times heart rate. Stroke volume is the volume of blood out of the ventricles per beat and if you multiply that times the heart rate, you get the volume out of the ventricles per minute, which is cardiac output.
7. You should be able to reproduce and use the equation relating cardiac output, stroke volume, and heart rate.
CO (vol/min) = SV (vol/beat) x HR (beat/min)
8. You should be able to identify the four determinants of cardiac output.
Contractility (force of contraction), preload (vol of blood that provides force in ventricles), afterload (force that heart has to overcome to get blood out and into circulation), and heart rate
9. You should be able to explain how each of the determinants affects cardiac output.
Contractility: the force with which the heart beats affects the volume of blood that is pumped out of the heart
Preload: the volume of blood in the ventricles, providing force against the myocardial affects the force with which the heart will contract (based on Frank-Sterling Law of the Heart)
Afterload: the force that the heart has to overcome in order to pump blood out of the heart and into circulation. If the vessel radius is decreased and there is more resistance to blood flow, the cardiac output will be reduced. Heart Rate - speeds up, CO increases (Sympathetic)... if decreased, HR decreases.
10. You should be able to state the Frank-Starling Law of the Heart.
The greater the muscle is stretched, the greater the force with which it will snap back
11. You should be able to explain the intrinsic and extrinsic controls over cardiac output
The extrinsic controls over cardiac output are those that rely on nervous system input. Contractility and heart rate are controlled extrinsically.
The intrinsic controls over cardiac output are preload (which is related to contractility) and afterload.
12. You should be able to explain in specific terms how sympathetic and parasympathetic input affect the determinants of cardiac output and therefore cardiac output itself.
Sympathetic ns input causes heart rate to increase which causes CO to increase. It also increases the contractility of the atria and the ventricles which increase CO. Parasympathetic ns input causes HR to decrease and therefore CO decreases. It also decreases the contractility of the atria which does not affect CO.
13. You should be able to explain what is meant by heart failure and why left-sided failure is more serious than right-sided.
Heart failure is any time CO decreases for any reason. Left-sided heart failure is more serious than right sided because the left side of the heart is responsible for delivering oxygenated blood to the body's systems. Also, if the left side of the heart is not pumping blood out while the right side is still working, blood begins to back up into the lungs and bulk flow causes excess amounts of fluids to accumulate in the lungs (congestion), which in turn causes a reduction in gas exchange. The body responds to the decreased CO by increasing HR and reabsorbing fluid in the kidneys. As blood volume increases, congestion worsens.
14. You should be able to explain the term "congestive" heart failure.
Congestive heart failure refers to the fact that when blood backs up into the lungs, fluid accumulates in the lung tissue, causing the lung tissue to become congested so that gas exchange is not as effective.
15. You should be able to discuss the diagnostic significance of LDL and HDL levels.
LDL (low density lipoprotein) and HDL (high density lipoprotein) are carriers for cholesterol in the circulatory system. LDL is considered "bad" because it dumps cholesterol in the blood vessels where it can accumulate and clog. HDL is considered "good" because it delivers cholesterol to the liver where it can be metabolized.
16. You should be able to identify and what affects the levels of LDLs and HDLs.
Genetics and Lifestyle. Good Genetics and lifestyle choices (diet, exercise) are the cause of higher levels of HDL's and lower levels of LDL's. Bad Genetics and lifestyle choices lead to lower HDL levels and higher LDL levels. HDL helps to rid the body of LDL (which makes plaque).
Stroke volume can be calculated by
subtracting the EsV from the EdV