knes2610 quiz 2/final

red blood

O2 rich, CO2 poor

blue blood

CO2 rich, O2 poor

2 circuits in parallel in the circulatory system

red blood and blue blood

what is also known as the mitral valve

bicuspid AV valve

steps of blood flow through the heart

• 1. Deoxygenated Blood Enters: Blood returns from the body and enters the right atrium via the superior and inferior vena cava.

• 2. Right Ventricle: Blood passes through the tricuspid valve into the right ventricle

  .

• 3. To the Lungs: The right ventricle pumps blood through the pulmonary valve into the pulmonary artery and to the lungs to receive oxygen.

• 4. Oxygenated Blood Returns: Oxygen-rich blood returns from the lungs to the left atrium via the pulmonary veins.

• 5. Left Ventricle: Blood moves through the mitral valve into the left ventricle.

• 6. To the Body: The left ventricle pumps oxygenated blood through the aortic valve into the aorta to circulate throughout the body.

what is the thicker ventricle, the left or right?

the left ventricle

why is the left ventricle thicker?

due to increased resistance due to increased pressure needed to pump oxygenated blood throughout the entire body

what is the proportion of blood in both the left and right ventricles

an equal amount of blood in each

what cardiac muscle features are found in skeletal muscle as well

striations

uni-nucleated

troponin (Calcium binding)

tropomyosin (covers myosin binding)

t-tubules

how are cardiac muscle cells connected?

by gap junctions and desosomes at the intercalated discs

SA node stands for

sino-atrial node

AV node stands for

atrio-ventricular node

what is the role of the SA and AV nodes?

they have pacemaker potential

pacemaker potential definition

Cyclic depolarizations of smooth and cardiac muscle that always reach threshold

pacemaker potential means no … is required

no nerve innervation is required

pacemaker potential involves the equilibrium potentials of…

EK+ = -94mv

ENa+ = +60mv

ECa2+ = +120mv

pacemaker potential meaning in regards to the SA node

the slow rise in membrane potential (depolarization) prior to an action potential in the SA node

Action potential

the rapid depolarization and repolarization that occur once the threshold is reached

what triggers an action potential in the heart?

the pacemaker gradually becoming less negative until it reaches the threshold to trigger the action potential

pacemaker potential sets what in the heart

the rhythm of the heart

If channels stand for

ion-funny channels

What is the first step in pacemaker potential?

the opening of the If channels, starting SA node depolarization.

how do Na+ and K+ ion permeabilities change at the start of SA node depolarization

K+ permeability decreases

Na+ permeability increases

how does Na+ move in/out cell at the start of SA node depolarization

a slow and constant inward leak

what occurs during the mid point of SA node depolarization

Ca2+ transient type voltage gated calcium ion channels open briefly as the pacemaker potential continues to rise toward threshold

what happens when the threshold pacemaker potential is reached

Long type Ca2+ channels open causing rapid depolarization and action potential

SA node is what kind of rhythmic and how?

autorhythmic because the series of events in an action potential keeps repeating itself

what happens at the end of a pacemaker action potential

L-type Ca2+ channels close and K+ channels open, allowing K+ to leave the cells of the SA node, thus repolarizing the SA node

state of various ion channels throughout the action potential

1. If channels open, starting depolarization at -60mv.

2. Some Ca2+ channels open, If channels close at around -50mv. Depolarization continues slowly.

3. Lots of Ca2+ channels open, causing rapid depolarization.

4. Ca2+ channels close, and K+ channels open once +20mv is reached, causing repolarization.

5. Once hyperpolarization has occurred, K+ channels close and If channels open, restarting the process.

initial period of spontaneous depolarization to subthreshold, ion channel gating and ion movement

Funny channels open, sodium moves in (dominantly) and potassium moves out

latter period of spontaneous depolarization to threshold, ion channel gating and ion movement

t-type calcium channels open and calcium moves in

rapid depolarization phase of action potential, ion channel gating and ion movement

L-type calcium channels open, calcium moves in

repolarization phase of action potential, ion channel gating and ion movement

potassium channels open, potassium moves out

impulses from the SA node are conducted through the atria at what speed

rapidly

impulses from SA node are conducted through the atria because of..

The gap junctions between muscle cells

what stimulates the atrial cells to contract

the wave of excitation

fibrous skeleton function

a dense collagenous connective tissue framework that anchors the four heart valves, separates the atria from the ventricles structurally, and acts as an electrical insulator, forcing impulses to pass only through the AV bundle for proper, synchronized contraction.

Where is the AV node located

another autorhythmic pacemaker found at the base of the right atrium, near the junction of the atria and ventricles

steps of the spread of depolarization through the heart

1. SA node depolarizes

2. electrical activity goes rapidly to AV node via internodal pathways

3. depolarization spreads more slowly across atria. conduction slows through AV node

4. depolarization rapidly moves through the ventricular conducting system to the apex of the heart

5. depolarization wave spreads upwards from the apex

impulses from the SA node are conducted where

to the AV node

AV node receives what from the SA node, and what does it do afterwards?

it receives the wave of excitation from the SA node, and transmits this wave to the ventricles.

AV noval delay

when the AV transmits the wave from the SA node to the ventricles, but with the signal delayed by about 100msec.

If channels are permeable to

Na+ and K+

wave of excitation spreads rapidly down where?

the left and right branches of the Bundle of His and the Purkinje fiber system.

the ventricular muscle undergoes… and develops an … when the wave of excitation reaches it.

it undergoes depolarization and develops and action potential

the conducting system of the heart contains

specialized cardiomyocytes, and fewer contractile filaments

what percentage of cells in the heart are in the conducting system

1%

AV node depolarizes at…

50bpm

SA node depolarizes at..

70 bpm

purkinje fibers depolarize at

35bpm

events in ventricular muscle action potential

stage 4- K+ permeable (efflux) at -90mv, impermeable to Na+ and Ca2+

stage 0- voltage gated Na+ channel fast channels open rapidly

stage 1- inactivation of Na+ channels at +20mv

1-2, brief opening of K+ channel

stage 2- opening of voltage gated calcium L-type channels = prolonged action potential plateau (increased calcium and decreased potassium permeability)

stage 3- L-type calcium channels close, K+ channels open leading to repolarization

stage 4- repeats

skeletal muscle fast twitch fiber refractory period/tension

the refractory period is very short compared with the amount of time required for tension development

skeletal muscle summation and tetanus

muscles stimulated repeatedly will exhibit summation and tetanus

cardiac muscle refractory period length and tetanus

the refractory period lasts almost as long as the entire muscle twitch, this long period in a cardiac muscle prevents tetanus (no summation)

myocardial muscle contraction steps

1. action potential enters from adjacent cell

2. voltage gated Ca2+ channels open, Ca2+ enters cell

3. Ca2+ induces Ca2+ release through ryanodine receptor channels

4. local release causes Ca2+ spark

5. summed Ca2+ sparks create a Ca2+ signal

6. Ca2+ ions bind to troponin to initiate contraction

7. relaxation occurs when Ca2+ unbinds from troponin

8. Ca2+ is pumped back into the sarcoplasmic reticulum for storage

9. Ca2+ is exchanged with Na+ by the NCX antiporter

10. Na+ gradient is maintained by the Na+-K+-ATPase

ECG- electrocardiogram

shows the function of the heart

Einthoven’s triangle

ECG electrodes attached to both arms and the leg form a triangle. each 2-electrode pair constitutes one lead with one positive and one negative electrode. an ECG is recorded from one lead at a time

P wave

atrial depolarization, initiated by the SA node

Q-R-S

depolarization of ventricles

T wave

ventricular repolarization

P-R segment

conduction through AV node, atria contracts, plateau/muscle cell contraction

S-T segment

ventricles contract

what is the cardiac cycle

a sequence of events that occurs in one heartbeat

cardiac cycle steps

1. late diastole- both sets of chambers are relaxed and ventricles fill passively

2. atrial systole- atrial contraction forces a small amount of additional blood into ventricles

3. heart sound (lub) because of tricuspid and bicuspid AV valves closing

4. isovolumic ventricular contraction- first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. Maximum volume of blood in ventricles = end diastolic volume (EDV)

5. ventricular ejection- as ventricular pressure rises and exceeds pressure in arteries, the semilunar valves open and blood is ejected

6. heart sound (dup) occurs as semilunar valves close once more

7. isovolumic ventricular relaxtion- as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed. minimum blood volume in ventricles = end-systolic volume (ESV)

EDV

end diastolic volume, maximum volume of blood in ventricles

ESV

end systolic volume, minimum volume of blood in ventricles

dicrotic notch

Closure of aortic semilunar valve

healthy blood pressure

120/80

stroke volume

the volume of blood pumped from the left ventricle of the heart per beat, typically measured in milliliters (mL)

stroke volume formula

EDV- ESV

end diostolic volume

The maximum volume of blood that the ventricles hold during a cardiac cycle

end systolic volume

The amount of blood left in the ventricle at the end of contraction

cardiac output

amount of blood ejected by the left or right ventricle per minute

cardiac output is a function of

Stroke volume and heartrate

cardiac ouput formula

SV x HR = ml/min

average cardiac output

5L/min

what division of the nervous system controls cardiac output

autonomic: parasympathetic and sympathetic

SA and AV nodes are controlled by input from the parasympathetic nervous system via…

the vagus nerve (CN X)

action of the parasympathetic system on cardiac output

1. acetylcoline binds to M2 recepter (muscarinic cholinergic)

2. activates Gi protein

3. decreases adenylate cyclase

4. decreases cAMP

5. increases K+ permeability, decreases Na+ permeability (funny channels), decreases Ca2+ (T-type channels)

6. hyperpolarizes pacemaker potential, decreasing heartrate

action of sympathetic system on cardiac output

1. norepinephrine/epinephrine binds to an adrenergic B1 receptor

2. stimulating Gs protein

3. increases adenylate cyclase

4. at SA node, K+ permeability decreases, Na+ permeability increases, and Ca2+ (T-type) increases

5. at AV node, decreased delay occurs

6. at Bundle of His and Purkinje system, faster conduction occurs

parasympathetic stimulation affect on HR

causes a decreased heartrate

sympathetic stimulation affect on HR

causes an increased HR

sympathetic system effect on myocardium

1. norepinephrine/epinephrine binds to an adrenergic B1 receptor

2. stimulating Gs protein

3. increases adenylate cyclase

4. increases cAMP

5. increased protein kinase A

6. protein kinase A phosphorylates SR Ca2+ channels, increasing intracellular release, allowing more binding of Ca2+ to troponin and enhanced actin myosin contraction, increasing cardiac muscle force and velocity (SV)

7. protein kinase A phosphorylates SR Ca2+ pumps, speeding Ca2+ removal and relaxation

8. protein kinase A phosprylates plasma membrane Ca2+ channels, increasing extracellular Ca2+ entry ( opening of more L-type channels)

Frank-Starling law of the heart revolves around…

intrinsic control of strength of myocardial contraction AKA length tension relationship

cardiac muscle optimal length tension relationship results in

increased stretch causing increased contraction permitting a match between EDV and SV

beyond optimal length tension relationship of cardiac muscle results in..

congestive heart failure

preload

influences EDV

the greater the EDV, the greater the…

SV

an increase in EDV causes…

SV to increase

impact of sympathetic stimulation on force and Frank-Starling law

increases SV for a given EDV, as EDV is influenced by preload

what factors cause increased stroke volume

• decreased arterial pressure (afterload)

• increased venous return → increased EDV

• increased sympathetic activity or epinephrine → increased contractility

what factors cause increased cardiac output

• increased activity of sympathetic nerves to heart → increased SV (ventricular myocardium) and increased heart rate (SA node)

• decreased activity of parasympathetic nerves to heart → increased heart rate (SA node)

heart muscle is highly … like slow twitch fibers

oxidative

why is heart muscle highly oxidative?

abundant mitochondria and myoglobin

main energy source of heart muscle

70% of energy is from fat oxidation

the heart relies on what for its supply of oxygen

coronary circulation

most of coronary blood flow takes place during…

diastole

systole has a drop in blood flow due to

squeezing of the heart muscle

coronary circulation steps

1. increased metabolic activity of cardiac muscle cells → increased oxygen need

2. increased adenosine

3. vasodilation of coronary vessels

4. increased blood flow to cardiac muscle cells

5. increased oxygen available to meet increased oxygen need