cardiovasc

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what does the cardiovascular system consist of?: -heart
-blood vessels
-blood
what's the function of the heart?: to allow the bulk flow of blood through pulmonary and systemic vascular systems.
what's the function of the blood vessels?: -blood transport
-blood pressure regulation
-exchange of gas/nutrients/wastes between cells and blood.
what's the function of the blood?: -gas/nutrient/waste transport
-protect from infection/cancer
-clotting
what is the -pericardium -epicardium: peri = fibrous sac enclosing the heart

epi = fibrous membrane on the surface of heart
what is between the epicardium and pericardium?: water to lubricate it.
what are the coronary arteries?: aa.s that supply blood to the myocardium
What ar the 4 requirements of the heart?: -maintain constant activity over lifetime
-can't fatigue
-must be regulatable and flexible in motor activity.
-maintain balance btwn pulmonary/systemic circulation.
what are the characteristics of cardiac muscle?: -only in heart
-involuntarily controlled
-single-nucleate
-electrically/mechanically couple to contract together.
-branched cells, striated.
what is unique about the junctions between cardiac muscle cells?: -joined by intercalated disks
-desmosomes inside disks hold cells together
what's the purpose of desmosomes?: -myofibrils of adjacent muscle cells attach to them
where are gap junctions in myocardium, and what are they for?: adjacent to intercalated disks; allow contact between conducting system and muscle cells.
why does myocardium have high mitochondria content?: for good aerobic metabolism.
-cardiac muscle can't build up an energy debt.
What does Functional Syncytium refer to?: the mechanical AND electrical coupling of cardiac muscle cells.
what supplies the -mechanical junction -electrical junction: mech: intercalated disks - strong.

elec: gap junctions - not strong.
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.
what are gap junctions made of?: membrane proteins - connexins - in adjacent membranes.

-when the connexins line up, it makes an ion channel through both membranes.
how do gap junctions function as electrical junctions?: when connexins lined up, ions can flow from cytoplasm of one cell to another, passing the action potential along.
what accounts for the mechanical strength of connections between cardiac muscle cells?: DESMOSOMES - proteins imbedded in the cells' plasma membranes.
what are the implications of desmosomes?: when one muscle cell contracts, it will mechanically pull on the cells on either side of it, making them contract too.
what is a desmosome made of?: -proteins imbedded in plasma membranes, anchored via
-Intermediate filaments.
-Attachment plaque increases stability.
what are the primary energy sources for cardiac muscle?: -aerobic metabolism
-LACTATE
-FATTY ACIDS
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.
What is the PRELOAD?: End-diastolic volume.
what is end-diastolic volume?: the volume of blood in the ventricles at the end of their filling (diastole).
what is AFTERLOAD?: the arterial pressures against which ventricles pump.
what 3 factors affect contraction force?: -Preload
-Sympathetic nervous system input changes
-Afterload (arterial pressure)
what does the Frank-Starling mechanism refer to?: the relationship between ventricular end-diastolic volume and stroke volume.
what IS the frank-starling mechanism?: Simple: as end-diastolic-volume increases, stroke volume increases.
More blood in, more blood out.
why does more blood go out when end-diastolic volume is increased?: because the ventricle muscles are more stretched, so their contraction generates more force.
What is Cardiac output?: the volume of blood pumped by EACH ventricle per minute
what does cardiac output equal?: Heartrate x stroke volume
HR x SV = CO
What happens to stroke volume and heartrate after blood loss?: Stroke volume decreases
Heartrate increases
what is the purpose of the Septum in the heart?: it provides electrical isolation between the two sides.
what is normal blood flow in the heart?: 5L/min
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.
What is the function of the heart valves?: -to permit unidirectional blood flow.

-to open/close based on pressure gradients.
What are the two AV valves names: -Tricuspid (right)
-Mitral (left)- only one with 2 cusps/leaflets.
what is the annulus?: a fibrous ring that encircles the valve
what are chordae tendinae?: fibrous ligaments that connect the leaflets to the papillary muscles.
what are papillary muscles for?: to stabilize the AV valves to prevent prolapse.

-Do NOT open/close valves.
which valves have a simpler structure, AV valves or semilunar?: semilunar.
what are the 2 semilunar valves?: -pulmonary

-aortic.
systole refers to what action of the ventricles and valves?: ventricular contraction.

period between mitral closing and aortic closing
during diastole what are the ventricles doing?: relaxing - filling with blood.
during isovolumetric ventricular contraction, how are the -atria/ventricles? -AV valve? -Aortic/pulmonary valves?: atria = relaxed,
ventric = contracting.

AV valve: closed
Semilunars: closed
during ventricular ejection, how are the -atria/ventricles? -AV valve? -Aortic/pulmonary valves?: atria: relaxed
ventricles: contracted
AV valve:closed
aorta/pulm valves: open
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.
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.
How many heart sounds are there?: 4 - S2, S2, S3, S4
what is the sound of: -S1 -S2: 1 = mitral valve closing - LUB

2 = semilunar valves closing - DUB
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
how much ventricular filling is atrial contraction responsible for?: only 20-30% - most just happens by ventricular relaxation.
what is diastasis?: atrial systole - reduced filling of that last 20-30% of ventricles. heard as S4 in heart sounds.
what is a heart murmur? 2 types of causes:: an abnormal sound caused by rapid blood flow.

2 causes: stenosis/insufficiency
what is stenosis?: -Narrowing of the valve opening.

-Causes pressure buildup behind the valve, so blood spurts out with more force -> more rapid flow.
When during a cardiac cycle is a stenosis heard? Does it cause any other alteration to valve closing?: when the valve is OPEN

no, the valve closes normally.
what is insuficciency?: when a valve doesn't close completely; it allows blood to regurgitate into where it came from.
when is insufficiency heard?: when the valve is closed (because blood is leaking back)

but the valve opens normally.
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.
what are the 2 systolic murmurs you might hear?: Semilunar stenosis
AV insufficiency
What are the 2 diastolic murmurs you might hear?: AV stenosis
Semilunar insufficiency
what are the names of 3 types of stenosis pathologies?: -bicuspid aortic valve
-senile aortic stenosis
-mitral stenosis
what is bicuspid aortic valve?: abnormality in the aortic valve so it's bi inst. of tricuspid. cuases restriction of blood flow, is Congenital.
What occurs in senile aortic stenosis?: the cusps become calcified and the valves are stiff and inflexible.
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.
what are 3 types of replacement valves for heart murmers?: -normal valves
-porcine or cadaveric replacements - last 15 yrs
-artificial replacements - they click.
what is the pacemaker of the heart?: the SA node
what is the SA node?: sinoatrial node - the pacemaker.
what pace does the SA node set?: 60-100 beats per min
what is the electrical link between the atria/ventricles?: the AV node.
what is the conductive nature of the AV node?: slow - it conducts the action potental very slowly - about 0.1 sec - so the ventricles contract AFTEr the atria
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.
how does contraction spread across the ventricles?: from Bottom to Top
what are purkinje fibers?: large, branching fibers that conduct action potential from r/l bundle branches to the myocardium
is myocardial conducting tissue Nerve tissue?: no!!! it's specialized myocardial cells that exhibit automaticity.
what is automaticity?: the lack of need for stimulation that is seen in myocardial cells.
how does electrical conduction spread through the heart during phase one?: begins at the SA node by symp or parasymp stimulation; atria excite; stimulates AV node; atria DONE.
how does electrical conduction spread through the heart during phase two?: 1. atria done while AV node still depolarizing.
2. AV stimulates bundle of His; then branches, then to purkinje fibers.
why are the atria done depolarizing by the time the ventricles start?: because Action potentials pass very slowly through the AV node.
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).
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.
what are L type Calcium channels?: voltage-gated Ca channels that allow a long-sustained influx when depolarized.
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.
what are inward rectifier channels?: potassium channels that open at highly negative potentials to allow outflow
what are delayed rectifier channels?: potassium channels that allow a sustained outflow when depolarized.
what are g-protein activated potassium channels?: channels that allow K+ outflow when activated by AcH or adenosine; important for neural regulation of heart rate.
what ion channel is the most important in functional beating?: the Funny channel
.: .
what are the two methods by which action potential can spread?: -via conducting tissue
-via myocardium through gap junctions.
which method does AP spread through the atria?: only through gap junctions.
what is the pacemaker potential?: the gradual/slow depolarization of the SA node that brings it to threshold for an action potential.
which 3 ion channels contribute to the pacemaker potential?: -Delayed rectifier K+ channels
-Funny Na+ channels
-Transient type Ca2+ channels
now what does automaticity mean?: 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.
what type of channel accounts for most of the depolarization in a conducting cell AP?: L-type Ca2+ channels opening
what type of channel accounts for repolarization to end an AP in conducting cells?: delayed rectifier K+ channels - allow K+ outflow
what starts the pacemaker potential?: delayed rectifier K+ channels closing
what two other channels account for the continued depolarization to cause a pacemaker potential?: -Funny channels allow Na influx when membrane potential is neg.

-T-type Ca channels allow CA influx top it off for the AP
How many phases are in Cardiac Action Potential generation in cardiac MUSCLE (not conduct. tissue)?: 5:
0 - upstroke,
1 - small repolariz.
2 - Plateau
3 - Repolarization
4 - back to resting potential.
what happens in phase 0?: Upstroke; Na+ fast channels open - normal, causes depolarization.
what happens in phase 1?: Small repolarization due to:

-Na+ channels close

-inward rectifier K+ channels open
what happens in phase 2?: Plateau - L-type Ca2+ channels open and calcium flows in to balance a closing of potassium inward rectifier channels.
what happens in phase 3?: Repolarization - delayed rectifier potassium channels open and allow efflux of K+
what happens in phase 4?: back to resting potential; inward rectifier K+ channels finish the job of returning to negative potential.
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.
what is -end-diastolic volume -end-systolic volume: EDV = volume in ventricle after ejection

ESV = volume in ventricle after filling
what is stroke volume?: the amount of blood ejected by EACH ventricle/beat, so

SV = EDV - ESV
what is ejection fraction?: SV/EDV x 100 - a percent.

Should be greater than 55%.
What is Cardiac Index?: the ratio of Cardiac Output to surface area.

CO/SA
What are the 3 ways to Physiologically control heart rate?: 1. Funny channels
2. Sympathetic nerv. system
3. Parasymp. nerv. system
What are Funny Channels?: Hyperpolariz.-activated cyclic nucleotide-gated channels. HCN
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.
how does the sympath. nerv system control heart rate?: -Enhances funny and Ca+ channels
-Inhibits K+ channels
-Increases heart rate
-Increases slope of pacemaker potential so AP is reached faster.
what neurotransmitters are used for the sympathetic control?: Norepinephrine - nerves release
Epinephrine - adrenal releases
what neurotransmitters are used for the parasympathetic control?: Acetylcholine from vagus nerve
How does parasymp nerv system control heart rate?: decreases it by doing the opposite of sympathetic.
what is -bradychardia -tachychardia -normal heart rate: normal = 60-100 beats/min
bradycardia is <60
tachychardia is >100
why do endurance athletes have lower normal heart rates?: their hearts are bigger stroke volume is higher and they don't need to pump as often.
how is STRENGTH of CONTRACTION increased?: by increasing
-afterload
-contractility
How is Contractility increased in the heart?: NOT by increasing EDV.

It is independent of EDV; use ionotropic agents.
Is the heart at its optimal length when normally pumping?: No - that's why increasing EDV increases Stroke Volume and the force generated with pumping.
Without changing EDV, how will increasing Aortic Pressure affect contractility?: It won't change contractility
Without changing EDV and contractility, how will increasing Aortic Pressure affect the strength of contraction? Stroke volume?: It will decrease both strength and stroke volume.
What is contractility?: The strength of contraction at any given end-diastolic volume.

INDEPENDENT of EDV.
What affects Contractility?: Ionotropic agents
what are 4 positive ionotropic agents?: 1. Catecholamines
2. Cardiac glycosides
3. High extracell. Ca2+
4. Low extracell Na+
what catecholamines increase contractility?: Epinephrine
Norepinephrine
Adrenergic agonists.
how do catecholamines affect contractility?: Myocardial cells have beta-adrenergic receptors that open calcium channels when stimulated with these NTs.
what are cardiac glycosides?: for example digitalis
how does digitalis increase contractility?: by decreasing Na/Ca ATPase
Intracell. Na increases
Pumping of Ca out decreases, so
Intracell. Ca increases.
What are the 5 steps in Cardiac Excitation-contraction coupling?: 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.
How is myocardial contraction terminated?: -by Ca ATPase reuptake into SR.
-by Ca ATPase in plasma memb.
-by Ca/Na exchanger pump
By maintaining the Ca/Na gradient.
What maximizes depolarization and contraction of the heart?: Intracellular - cytosolic Ca2+.

Because the cells are mech. linked, cannot recruit cells.
Must use Ca2+ concentration
What increases Myocardial Contraction Strength?: Cytosolic calcium
What are 3 negative ionotropic agents?: -Calcium channel blockers
-High extracell Na
-Low intracell Ca
What is a calcium channel blocker?: verapamil
what does Verapamil do?: Decreases Ca2+ influx during the plateau phase of the myocardial action potential.
What type of channel does Verapamil block?: L-type Ca2+ channels.
What happens to contractility as heart rate increases?: Contractility increases because intracellular Ca2+ increases.
SUMMARY: CO = HR x SV and -HR is affected by -SV is affected by:: HR: sympathetic or parasymp nervous activity

SV: EDV or contractility
what is cardiomyopathy?: a group of diseases that affect heart MUSCLE and cause decreased contractility.
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.
what is heart failure caused by?: ventricular remodeling.
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
what is the body's response to decreased SV in heart failure?: to increase blood volume - retains fluid.
How does heart failure affect EDV?: severely decreased, even with fluid retention.

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