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148 Cards in this Set
- Front
- Back
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what does the cardiovascular system consist of?
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-heart
-blood vessels -blood |
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what's the function of the heart?
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to allow the bulk flow of blood through pulmonary and systemic vascular systems.
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what's the function of the blood vessels?
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-blood transport
-blood pressure regulation -exchange of gas/nutrients/wastes between cells and blood. |
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what's the function of the blood?
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-gas/nutrient/waste transport
-protect from infection/cancer -clotting |
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what is the
-pericardium -epicardium |
peri = fibrous sac enclosing the heart
epi = fibrous membrane on the surface of heart |
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what is between the epicardium and pericardium?
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water to lubricate it.
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what are the coronary arteries?
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aa.s that supply blood to the myocardium
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What ar the 4 requirements of the heart?
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-maintain constant activity over lifetime
-can't fatigue -must be regulatable and flexible in motor activity. -maintain balance btwn pulmonary/systemic circulation. |
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what are the characteristics of cardiac muscle?
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-only in heart
-involuntarily controlled -single-nucleate -electrically/mechanically couple to contract together. -branched cells, striated. |
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what is unique about the junctions between cardiac muscle cells?
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-joined by intercalated disks
-desmosomes inside disks hold cells together |
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what's the purpose of desmosomes?
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-myofibrils of adjacent muscle cells attach to them
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where are gap junctions in myocardium, and what are they for?
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adjacent to intercalated disks; allow contact between conducting system and muscle cells.
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why does myocardium have high mitochondria content?
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for good aerobic metabolism.
-cardiac muscle can't build up an energy debt. |
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What does Functional Syncytium refer to?
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the mechanical AND electrical coupling of cardiac muscle cells.
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what supplies the
-mechanical junction -electrical junction |
mech: intercalated disks - strong.
elec: gap junctions - not strong. |
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what is the SR like in cardiac compared to skeletal muscle?
What is its purpose? |
less extensive, but still releases Ca+ for contraction.
action potential causes it to release calcium inside the cell. |
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what are gap junctions made of?
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membrane proteins - connexins - in adjacent membranes.
-when the connexins line up, it makes an ion channel through both membranes. |
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how do gap junctions function as electrical junctions?
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when connexins lined up, ions can flow from cytoplasm of one cell to another, passing the action potential along.
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what accounts for the mechanical strength of connections between cardiac muscle cells?
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DESMOSOMES - proteins imbedded in the cells' plasma membranes.
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what are the implications of desmosomes?
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when one muscle cell contracts, it will mechanically pull on the cells on either side of it, making them contract too.
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what is a desmosome made of?
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-proteins imbedded in plasma membranes, anchored via
-Intermediate filaments. -Attachment plaque increases stability. |
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what are the primary energy sources for cardiac muscle?
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-aerobic metabolism
-LACTATE -FATTY ACIDS |
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where does the heart get -lactate
-fatty acids -other |
lactate - carb from skeletal muscle activity.
fatty acids - from stored fat degradation. -ketone bodies, amino acids - from fat degradation. |
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What is the PRELOAD?
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End-diastolic volume.
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what is end-diastolic volume?
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the volume of blood in the ventricles at the end of their filling (diastole).
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what is AFTERLOAD?
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the arterial pressures against which ventricles pump.
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what 3 factors affect contraction force?
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-Preload
-Sympathetic nervous system input changes -Afterload (arterial pressure) |
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what does the Frank-Starling mechanism refer to?
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the relationship between ventricular end-diastolic volume and stroke volume.
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what IS the frank-starling mechanism?
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Simple: as end-diastolic-volume increases, stroke volume increases.
More blood in, more blood out. |
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why does more blood go out when end-diastolic volume is increased?
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because the ventricle muscles are more stretched, so their contraction generates more force.
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What is Cardiac output?
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the volume of blood pumped by EACH ventricle per minute
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what does cardiac output equal?
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Heartrate x stroke volume
HR x SV = CO |
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What happens to stroke volume and heartrate after blood loss?
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Stroke volume decreases
Heartrate increases |
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what is the purpose of the Septum in the heart?
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it provides electrical isolation between the two sides.
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what is normal blood flow in the heart?
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5L/min
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on which side of the heart is
-pressure higher -resistance higher -How can you tell? |
Both pressure and resistance are higher on the left side of the heart.
-Left side has much thicker ventricular wall. |
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What is the function of the heart valves?
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-to permit unidirectional blood flow.
-to open/close based on pressure gradients. |
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What are the two AV valves names
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-Tricuspid (right)
-Mitral (left)- only one with 2 cusps/leaflets. |
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what is the annulus?
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a fibrous ring that encircles the valve
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what are chordae tendinae?
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fibrous ligaments that connect the leaflets to the papillary muscles.
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what are papillary muscles for?
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to stabilize the AV valves to prevent prolapse.
-Do NOT open/close valves. |
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which valves have a simpler structure, AV valves or semilunar?
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semilunar.
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what are the 2 semilunar valves?
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-pulmonary
-aortic. |
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systole refers to what action of the ventricles and valves?
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ventricular contraction.
period between mitral closing and aortic closing |
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during diastole what are the ventricles doing?
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relaxing - filling with blood.
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during isovolumetric ventricular contraction, how are the
-atria/ventricles? -AV valve? -Aortic/pulmonary valves? |
atria = relaxed,
ventric = contracting. AV valve: closed Semilunars: closed |
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during ventricular ejection, how are the
-atria/ventricles? -AV valve? -Aortic/pulmonary valves? |
atria: relaxed
ventricles: contracted AV valve:closed aorta/pulm valves: open |
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during isovolumetric ventricular relaxation, how are the
-atria/ventricles? -AV valve? -Aortic/pulmonary valves? |
atria and ventricles: relaxed
av valve: closed aortic/pulmon. valves: closed. |
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during ventricular filling, how are the
-atria/ventricles? -AV valve? -Aortic/pulmonary valves? |
atria: contracts after initial filling
ventricles: relaxed av valve: open aortic/pulmon. valves: closed. |
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How many heart sounds are there?
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4 - S2, S2, S3, S4
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what is the sound of:
-S1 -S2 |
1 = mitral valve closing - LUB
2 = semilunar valves closing - DUB |
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if you can hear S3 and S4, what does that mean?
what are these sounds? |
it's indicative of disease.
s3 = rapid filling of ventricles S4 = atrial systole (contraction), reduced filling |
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how much ventricular filling is atrial contraction responsible for?
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only 20-30% - most just happens by ventricular relaxation.
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what is diastasis?
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atrial systole - reduced filling of that last 20-30% of ventricles. heard as S4 in heart sounds.
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what is a heart murmur?
2 types of causes: |
an abnormal sound caused by rapid blood flow.
2 causes: stenosis/insufficiency |
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what is stenosis?
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-Narrowing of the valve opening.
-Causes pressure buildup behind the valve, so blood spurts out with more force -> more rapid flow. |
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When during a cardiac cycle is a stenosis heard? Does it cause any other alteration to valve closing?
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when the valve is OPEN
no, the valve closes normally. |
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what is insuficciency?
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when a valve doesn't close completely; it allows blood to regurgitate into where it came from.
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when is insufficiency heard?
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when the valve is closed (because blood is leaking back)
but the valve opens normally. |
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what is louder,
a systolic murmer? or a diastolic murmer? |
a systolic - that's when the ventricles are contracting and blood is pushed out the semilunar valves at a higher flowrate, big sound.
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what are the 2 systolic murmurs you might hear?
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Semilunar stenosis
AV insufficiency |
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What are the 2 diastolic murmurs you might hear?
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AV stenosis
Semilunar insufficiency |
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what are the names of 3 types of stenosis pathologies?
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-bicuspid aortic valve
-senile aortic stenosis -mitral stenosis |
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what is bicuspid aortic valve?
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abnormality in the aortic valve so it's bi inst. of tricuspid. cuases restriction of blood flow, is Congenital.
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What occurs in senile aortic stenosis?
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the cusps become calcified and the valves are stiff and inflexible.
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what is mitral stenosis?
what can be a cause? |
when the mitral valve doesn't open enough.
-may be due to bacterial inf. or rheumatic disease. |
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what are 3 types of replacement valves for heart murmers?
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-normal valves
-porcine or cadaveric replacements - last 15 yrs -artificial replacements - they click. |
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what is the pacemaker of the heart?
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the SA node
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what is the SA node?
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sinoatrial node - the pacemaker.
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what pace does the SA node set?
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60-100 beats per min
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what is the electrical link between the atria/ventricles?
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the AV node.
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what is the conductive nature of the AV node?
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slow - it conducts the action potental very slowly - about 0.1 sec - so the ventricles contract AFTEr the atria
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what are bundle branches?
what do they do? |
branches that come off the bundle of His; deliver impulse simultaneously to the R and L ventricles.
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how does contraction spread across the ventricles?
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from Bottom to Top
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what are purkinje fibers?
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large, branching fibers that conduct action potential from r/l bundle branches to the myocardium
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is myocardial conducting tissue Nerve tissue?
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no!!! it's specialized myocardial cells that exhibit automaticity.
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what is automaticity?
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the lack of need for stimulation that is seen in myocardial cells.
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how does electrical conduction spread through the heart during phase one?
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begins at the SA node by symp or parasymp stimulation; atria excite; stimulates AV node; atria DONE.
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how does electrical conduction spread through the heart during phase two?
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1. atria done while AV node still depolarizing.
2. AV stimulates bundle of His; then branches, then to purkinje fibers. |
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why are the atria done depolarizing by the time the ventricles start?
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because Action potentials pass very slowly through the AV node.
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what are Ina channels?
In what type of myocardium are Ina channels found? |
Channels that allow fast Na influx if depolarized. Inactivate rapidly
ONLY in working, contractile. Not in conductive tissue (SA or AV nodes). |
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what are If channels?
In what type of myocardium are they found? |
funny channels that allow a slow leak of Na into the cell when they are hyperpolarized.
ONLY found in conductive tissue. |
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what are L type Calcium channels?
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voltage-gated Ca channels that allow a long-sustained influx when depolarized.
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what are T type Calcium channels?
in what type of tissue? |
channels that allow a transient influx of CA when depolarized; only found in conducting tissue.
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what are inward rectifier channels?
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potassium channels that open at highly negative potentials to allow outflow
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what are delayed rectifier channels?
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potassium channels that allow a sustained outflow when depolarized.
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what are g-protein activated potassium channels?
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channels that allow K+ outflow when activated by AcH or adenosine; important for neural regulation of heart rate.
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what ion channel is the most important in functional beating?
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the Funny channel
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.
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what are the two methods by which action potential can spread?
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-via conducting tissue
-via myocardium through gap junctions. |
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which method does AP spread through the atria?
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only through gap junctions.
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what is the pacemaker potential?
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the gradual/slow depolarization of the SA node that brings it to threshold for an action potential.
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which 3 ion channels contribute to the pacemaker potential?
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-Delayed rectifier K+ channels
-Funny Na+ channels -Transient type Ca2+ channels |
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now what does automaticity mean?
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it refers to the fact that conducting cells don't have a resting memb. potential, but have a rythmic pattern of pot. alteration by different channels opening/closing.
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what type of channel accounts for most of the depolarization in a conducting cell AP?
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L-type Ca2+ channels opening
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what type of channel accounts for repolarization to end an AP in conducting cells?
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delayed rectifier K+ channels - allow K+ outflow
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what starts the pacemaker potential?
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delayed rectifier K+ channels closing
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what two other channels account for the continued depolarization to cause a pacemaker potential?
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-Funny channels allow Na influx when membrane potential is neg.
-T-type Ca channels allow CA influx top it off for the AP |
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How many phases are in Cardiac Action Potential generation in cardiac MUSCLE (not conduct. tissue)?
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5:
0 - upstroke, 1 - small repolariz. 2 - Plateau 3 - Repolarization 4 - back to resting potential. |
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what happens in phase 0?
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Upstroke; Na+ fast channels open - normal, causes depolarization.
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what happens in phase 1?
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Small repolarization due to:
-Na+ channels close -inward rectifier K+ channels open |
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what happens in phase 2?
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Plateau - L-type Ca2+ channels open and calcium flows in to balance a closing of potassium inward rectifier channels.
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what happens in phase 3?
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Repolarization - delayed rectifier potassium channels open and allow efflux of K+
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what happens in phase 4?
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back to resting potential; inward rectifier K+ channels finish the job of returning to negative potential.
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what is the purpose of the refractory period in cardiac muscle?
When is this period? |
to allow ventricles time to fill, and to prevent tetanus.
Time: from action potential until completely repolarized. |
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what is
-end-diastolic volume -end-systolic volume |
EDV = volume in ventricle after ejection
ESV = volume in ventricle after filling |
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what is stroke volume?
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the amount of blood ejected by EACH ventricle/beat, so
SV = EDV - ESV |
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what is ejection fraction?
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SV/EDV x 100 - a percent.
Should be greater than 55%. |
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What is Cardiac Index?
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the ratio of Cardiac Output to surface area.
CO/SA |
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What is Cardiac Output?
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Stroke volume x Heart rate
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What are the 3 ways to Physiologically control heart rate?
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1. Funny channels
2. Sympathetic nerv. system 3. Parasymp. nerv. system |
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What are Funny Channels?
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Hyperpolariz.-activated cyclic nucleotide-gated channels. HCN
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How do funny channels control heart rate?
What stimulates them? |
they have the greatest influence on SA node firing rate, and so the heart rate.
Stimulated by cyclic AMP. |
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how does the sympath. nerv system control heart rate?
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-Enhances funny and Ca+ channels
-Inhibits K+ channels -Increases heart rate -Increases slope of pacemaker potential so AP is reached faster. |
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what neurotransmitters are used for the sympathetic control?
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Norepinephrine - nerves release
Epinephrine - adrenal releases |
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what neurotransmitters are used for the parasympathetic control?
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Acetylcholine from vagus nerve
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How does parasymp nerv system control heart rate?
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decreases it by doing the opposite of sympathetic.
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what is
-bradychardia -tachychardia -normal heart rate |
normal = 60-100 beats/min
bradycardia is <60 tachychardia is >100 |
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why do endurance athletes have lower normal heart rates?
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their hearts are bigger stroke volume is higher and they don't need to pump as often.
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how is STRENGTH of CONTRACTION increased?
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by increasing
-afterload -contractility |
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How is Contractility increased in the heart?
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NOT by increasing EDV.
It is independent of EDV; use ionotropic agents. |
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Is the heart at its optimal length when normally pumping?
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No - that's why increasing EDV increases Stroke Volume and the force generated with pumping.
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Without changing EDV, how will increasing Aortic Pressure affect contractility?
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It won't change contractility
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Without changing EDV and contractility, how will increasing Aortic Pressure affect the strength of contraction? Stroke volume?
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It will decrease both strength and stroke volume.
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What is contractility?
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The strength of contraction at any given end-diastolic volume.
INDEPENDENT of EDV. |
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What affects Contractility?
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Ionotropic agents
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what are 4 positive ionotropic agents?
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1. Catecholamines
2. Cardiac glycosides 3. High extracell. Ca2+ 4. Low extracell Na+ |
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what catecholamines increase contractility?
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Epinephrine
Norepinephrine Adrenergic agonists. |
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how do catecholamines affect contractility?
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Myocardial cells have beta-adrenergic receptors that open calcium channels when stimulated with these NTs.
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what are cardiac glycosides?
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for example digitalis
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how does digitalis increase contractility?
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by decreasing Na/Ca ATPase
Intracell. Na increases Pumping of Ca out decreases, so Intracell. Ca increases. |
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What are the 5 steps in Cardiac Excitation-contraction coupling?
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1. Plasma membrane depolarizes.
2. Vltg stimulates Ca2+ channels in T-tubules to open 3. Ca2+ binds SR calcium channels 4. SR releases Ca2+ to cytosol 5. Ca2+ binds troponin, causes a POWER STROKE. |
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How is myocardial contraction terminated?
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-by Ca ATPase reuptake into SR.
-by Ca ATPase in plasma memb. -by Ca/Na exchanger pump By maintaining the Ca/Na gradient. |
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What maximizes depolarization and contraction of the heart?
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Intracellular - cytosolic Ca2+.
Because the cells are mech. linked, cannot recruit cells. Must use Ca2+ concentration |
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What increases Myocardial Contraction Strength?
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Cytosolic calcium
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What are 3 negative ionotropic agents?
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-Calcium channel blockers
-High extracell Na -Low intracell Ca |
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What is a calcium channel blocker?
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verapamil
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what does Verapamil do?
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Decreases Ca2+ influx during the plateau phase of the myocardial action potential.
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What type of channel does Verapamil block?
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L-type Ca2+ channels.
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What happens to contractility as heart rate increases?
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Contractility increases because intracellular Ca2+ increases.
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SUMMARY: CO = HR x SV and
-HR is affected by -SV is affected by: |
HR: sympathetic or parasymp nervous activity
SV: EDV or contractility |
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what is cardiomyopathy?
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a group of diseases that affect heart MUSCLE and cause decreased contractility.
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What is cardiomyopathy in young athletes?
what causes it? What is the result? |
hypertrophic cardiomyopathy
-caused by thickening of ventricular walls and septum -results in fibrillation. |
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what is heart failure caused by?
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ventricular remodeling.
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how does the heart change in:
-diastolic heart failure -systolic heart failure |
diast: hypertropied heart - walls thicken and SV is decr.
syst: dilated heart to compensate for diast failure; results in decreased SV |
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what is the body's response to decreased SV in heart failure?
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to increase blood volume - retains fluid.
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How does heart failure affect EDV?
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severely decreased, even with fluid retention.
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