BIOL 5600 Exam 3 Cardiovascular I

cardiovascular system functions

- transport system

- immune defense

- acid-base balance

- fluid balance

cardiovascular transport

moves O2, CO2, nutrients, hormones, and wastes

cardiovascular immune defense

transports WBCs and other immune components

cardiovascular acid-base balance

helps regulate blood pH by transporting CO2, which affects acidity

cardiovascular fluid balance

helps distribute fluid between plasma and tissues

main cardiovascular components

1. heart (the pump)

2. blood vessels (the pipes)

3. blood (the transport fluid)

the heart

pumps blood through the pulmonary and systemic circuits

blood vessels

arteries, veins, capillaries

arteries

carry blood away from the heart

veins

carry blood toward heart

capillaries

tiny vessels where substances are exchanged between blood and tissues

blood components

plasma, RBCs, WBCs, platelets

plasma

liquid portion of blood

red blood cells

transport oxygen

white blood cells

help defend against infection

platelets

help blood clot

chambers of the heart

right atrium, right ventricle, left atrium, left ventricle

right atrium

receives oxygen-poor blood from body

right ventricle

pumps oxygen-poor blood to lungs

left atrium

receives oxygen-rich blood from lungs

left ventricle

pumps oxygen-rich blood to body

blood pathway

1. right atrium

2. tricuspid valve

3. right ventricle

4. pulmonary semilunar valve

5. pulmonary arteries

6. lung capillaries

7. pulmonary veins

8. left atrium

9. bicuspid

10. left ventricle

11. aortic semilunar valve

12. aorta / systemic arties

13. systemic capillaries

14. systemic veins

15. inferior vena cava

lung capillaries

blood releases CO2 and picks up O2

systemic capillaries

deliver O2 and nutrients to tissues; collect CO2 and wastes

pulmonary circuit

- right heart --> lungs --> left heart

- sends oxygen-poor blood to lungs

- gas exchange occurs in lung capillaries

- returns oxygen-rich blood to left atrium

systemic circuit

- left heart --> body --> right heart

- sends oxygen-rich blood to body

- body capillaries exchange O2, nutrients, and wastes

- returns oxygen-poor blood to right atrium

coronary circuit

- aorta --> heart muscle --> right atrium

- supplies myocardium with oxygen and nutrients

- coronary arteries branch from aorta

- cardiac veins collect blood from heart muscle and drain mainly into coronary sinus, which empties into right atrium

cardiac muscle cell types

contractile tissue and conductive tissue

contractile tissue

- 99% of heart wall

- contracts and generates force

- atria and ventricles

- DCT between atria and ventricles

atria

- 2, right and left

- smaller, thin walled, separated by septum

- contractile chambers

- not much contractile force

ventricles

- 2, right and left

- much larger, very thick walled, separated by septum

- contractile chambers

- lots of contractile force

deep connective tissue

- between atria and ventricles

- "skeleton of the heart"

- holds valves (AV and semilunar)

- cause atria and ventricles to act as TWO functional synctitia

- atria contract as unit, ventricles contract as unit

conductive tissue

- autonomously initiates electrical events and disperses them to contractile cells

- conducts and distributes electrical signals to contractile cells

- coordinates timing of heart contractions

- intrinsic conduction system

- specialized myocytes

- NOT contractile

- intrinsic waves of depolarization/repolarization

- heart keeps beating without nervous input

- sympathetic and parasympathetic input ALTER this intrinsic rhythym

intrinsic conduction system

- pathway that carries electrical signals through the heart in a specific order

- clusters/fibers of conductive cells

- part of myocardium

1. SA node

2. atrial pathways

3. AV node

4. bundle of His

5. left and right bundle branches

6. purkinje fibers

SA node

- first part of intrinsic conduction system

- right atrium

- starts electrical impulse

- natural pacemaker

- FASTEST rate of intrinsic depolarization/repolarization

- rate swamps out others so every conductive cell adopts SA node's rhythm

- just below entrance of superior vena cava

- generates impulses ~ 70-75 times/minute

- signal spreads via the internodal pathway

- from contractile cell to contractile cell via intercalated discs (gap junctions)

atrial pathways

- second part of intrinsic conduction system

- internodal pathways carry signal toward AV node

- Bahmani's bundle carries signal to left atrium

AV node

- third part of intrinsic conduction system

- right atrium

- briefly delays impulse so ventricles can fill (0.1 seconds)

- second fastest rate of depol/repol

- bottom of right atrium

- where signal resynchronizes

- delay due to smaller fiber diameter and fewer gap junctions

- allows atria to respond and complete their contraction before ventricles contract

bundle of His

- fourth part of intrinsic conduction system

- aka AV bundle

- carries impulse toward ventricles

- slowest rate of depol/repol

- impulse travels fast again here after delay at AV node

- runs down interventricular septum

- only way (usually) between atria and ventricles due to heart skeleton

left and right bundle branches

- fifth part of intrinsic conduction system

- carry impulse down interventricular septum toward each ventricle

purkinje fibers

- final part of intrinsic conduction system

- rapidly distributes the impulse throughout the ventricular myocardium (depolarizes contractile cells)

- aka subendocardial conducting network

- ventricle walls thicker than atria, and left ventricle thicker than right

- NEED PURKINJE FIBERS to spread signal EFFICIENTLY

intrinsic conduction system order

1. SA node fires

- electrical impulse begins and atria are activated

- impulses travel from SA node to ALL atrial cells via gap junctions ("internodal pathway")

2. atria contract

- blood moves from atria into ventricles

3. AV node delays

- gives ventricles time to fill

4. impulse travels down Bundle of His, bundle branches, and Purkinje fibers

5. ventricles contract

- blood is ejected into pulmonary artery and aorta

contractile cardiac muscle cells

- short, branched, square-shaped cells

- striated, with contractile proteins in sarcomeres

- involuntary

- sarcomeres

- actin, myosin, troponin, tropomyosin

- intercalated discs, desmosomes, gap junctions

intercalated discs

- specialized connections between adjacent cardiac muscle cells

- help heart contract as coordinated unit

gap junction

- aligned channels pass ions and small molecules directly between cytoplasms

- allow ions and electrical signals to pass directly between neighboring cells

- help action potential spread and coordinate cardiac muscle contraction

desmosome

- a spot-like cell-cell anchor links intermediate filaments to resist tensile stress

- hold neighboring cardiac muscle cells together

- prevent cells from pulling apart during repeated

functional syncytium

- cardiac muscle cells act as coordinated unit because of gap junctions

- do not need individual nerve stimulation to initiate heartbeat bc heart has own conduction system

mitochondria

make up 25-35% of cardiac muscle cell volume (versus only 2% in skeletal muscle cell volume)

myoglobin

stores oxygen inside muscle cells

glycogen

provides stored glucose for energy production

why is cardiac muscle fatigue resistant?

- large supply of mitochondria, myoglobin, and glycogen

- heart contracts continually, so needs large supply of ATP

- mitochondria and oxygen supply help produce energy aerobically and make it fatigue-resistant

sarcoplasmic reticulum

- stores Ca2+ ions

- Ca2+ released into cell to initiate contraction

- cardiac muscle has SIMPLER sarcoplasmic reticulum than skeletal muscle

- cardiac SR lacks large terminal cisternae found in skeletal muscle, but has more developed SR than smooth muscle

t-tubules

- carry electrical depolarization from cell surface to muscle cell interior

- cardiac t-tubules are 5x wide than skeletal

- cardiac has less t-tubules than skeletal

cardiac contractile cell action potential

- long absolute refractory period (~ 200 ms)

- CANNOT tetanize

- action potential length = ~ 250 ms

- resting potential -90 to -95 mV

cardiac muscle cell contraction

- Phase 0: depolarization

- Phase 1

- Phase 2: plateau phase

- Phase 3

cardiac muscle cell depolarization

- phase 0

- FAST VR Na+ channels OPEN

- peak at +20 - +30 mV

phase 1 (cardiac muscle cell contraction)

- INACTIVATION of FAST VR Na+ channels

- one population VR K+ channels (inward rectifier channels !!) initially slowly open

- some K+ starts moving out of the cells start an INITIAL repolarization

- BUT then these VR K+ channels slowly close, reducing this permeability

inward rectifier channels

- population of VR K+ channels that open INITIALLY in phase 1 of cardiac muscle contraction

- reopen in phase 3 to increase repolarization

cardiac muscle cell plateau phase (phase 2)

- VR SLOW Ca2+ channels start to open

- keep it depolarized, causes plateau

phase 3 (cardiac muscle cell contraction)

- as VR SLOW Ca2+ close, another population of slow VR K+ channels open, DELAYED rectifier channels REPOLARIZES action potential (started opening in phase 1 and 2 but very slow)

- repolarization causes inward rectifier channels that were closed during phase 1 to also open, increasing the repolarization

- Ca2+ is pumped back into SR and outside in repolarization

calcium-induced calcium release (CICR)

in cardiac muscle cells, calcium entering cell trigger release of more Ca2+ from sarcoplasmic reticulum

CICR process

1. depolarization occurs

- AP travels on cardiomyocyte membrane

- signal travels down T-tubules

- depolarization opens L-type calcium channels

2. calcium enters cell

- L-type calcium channels open

- Ca2+ enters cell from ECF

- initial calcium entry = TRIGGER CALCIUM (tells SR to release more Ca2+)

3. CICR

- incoming Ca2+ activates ryanodine receptors (RyR) on SR

- RyR open and release stored Ca2+ from SR into cytoplasm

4. contraction

- cross-bridge cycling

- more intracellular Ca2+ --> increased force of contraction

5. relaxation: calcium is removed from cytoplasm

- main mechanism: SERCA pump

- calcium detaches from troponin

- tropomyosin covers myosin binding sites again

- cross bridge cycling stops

ryanodine receptors

- calcium release channels on sarcoplasmic reticulum

- incoming Ca2+ from L-type calcium channels activates them

- release stored Ca2+ from SR into cytoplasm

SERCA pump

- sarcoplasmic/endoplasmic reticulum Ca2+-ATPase

- uses ATP to pump Ca2+ from cytoplasm back to SR

- main mechanism of cardiac muscle cell relaxation

calcium in cardiac vs. skeletal muscle

- cardiac: Ca2+ entering cell triggers Ca2+ release from SR

- skeletal: voltage-sensing receptors mechanically trigger Ca2+ release from SR

calcium channel blockers

- block L-type calcium channels

1. less Ca2+ enters cell

2. less CICR occurs

3. intracellular Ca2+ decreases

4. contraction force decreases

- decreased contractility --> decreased stroke volume

epinephrine and norepinephrine

enhance Ca2+ delivery (sympathetic), increasing HR and stroke volume

electrical excitation sequence

1. SA node generates impulses

2. impulse pauses (0.1 s) at AV node

3. AV bundle connects atria to ventricles

4. bundle branches conduct impulses through interventricular septum

5. Purkinje fibers depolarizes the contractile cells of both ventricles

conductive cell action potential

- different than contractile cell AP (NO STABLE RESTING POTENTIAL)

- "resting" potential is unstable --> called prepotential/pacemaker potential

- not as polarized as contractile tissue ~ -60 mV

- threshold is ~ -40 to -50 mV

- AP --> VR Ca2+ channels open

- goes to just above 0 mV before repolarizes

prepotential (pacemaker potential / "funny current")

- first part of CONDUCTIVE cell action potential

- slow depolarization due to opening of Na+ channels, closing of K+ channels

- K+ permeability decreases, Na+ permeability increases

- SLOW Na+ channels open

- membrane potential NEVER a flat line

Conductive Cell Action Potential Step 2

- -40 mV threshold

- FAST VR Ca2+ channels

- AP depolarization

Conductive Cell Action Potential Step 3

- above 0 mv

- FAST VR Ca2+ channels close and inactivate

- VR K+ channels open (repolarization)

- as K+ channels close, "funny current" causes SLOW Na+ to start opening

sympathetic NS input on cardiac conductive cell

- causes STEEPER prepotential

- faster climb to threshold --> faster heart rate

parasympathetic NS input on cardiac conductive cell

- FLATTER prepotential

- takes longer to reach threshold --> slower heart rate

heart transplant

without nervous input intrinsic rate of depolarization/repolarization rises to 100 bpm

why doesn't electrical signal go straight to ventricles?

- dense connective tissue between atria and ventricles

- "insulator" of the heart

- hold right and left AV valves, right and left semilunar valves

conduction system time

total time between impulse initiation (SA node) to depolarization of last ventricular fiber is 0.22 s (220 ms)

p wave

- atrial depolarization (ECG)

- 0.8 s (80 ms)

- atrial depolarization spread from SA node to atria

- approximately 0.1 s (100 ms) after p wave BEGINS, atria contract

QRS wave

- ventricular depolarization (--> ventricular contraction)

- atria depolarize here as well, but weaker electrical deviation so is masked by ventricular depolarization

- 80 ms

- depolarization starts at apex, goes to right ventricle, then runs from inner to outer walls through ventricles, then ventricles contract

t wave

- ventricular repolarization (--> ventricular relaxation)

- occurs just BEFORE ventricles start to relax

- lasts 160 ms

- repolarization takes longer, more drawn out and flatter

depolarization rates

- different parts of conduction system have different depolarization rates

- SA node: driving heart to be ~70-75 bpm

- no SA node --> AV node: 50 bpm (enough to sustain circulation but slow)

- no AV node --> bundle of His, branches, purkinje fibers

- spontaneously depol/repol for 30 bpm (NOT ENOUGH TO SUSTAIN LIFE)

- slower pacemakers don't dominate if SA is functioning

- no conduction system (AV bundle and purkinje fibers) signal travels at 0.3 - 0.5 meters/s vs several meters/s

arrythmias

- irregular heart rhythms

- uncoordinated atrial/ventricular contractions

fibrillation

- condition of rapid and irregular / out of phase contractions

- control away from SA node by rapid, uncoordinated activity in other areas

- multiple circus movements are occurring

- little clusters of cells are all doing their own thing --> anarchy fo events

defibrillation

- electric shocking of heart

- depolarizing ALL the myocardium

- interrupts chaotic twitching

- slate wiped clean and SA node can recover control of rhythm

defective SA node

- consequences

- ectopic focus

- AV node may become pacemaker (40-60 bpm)

- sometimes ectopic pacemakers appear even if SA node is okay

- part of muscle gets hyper-excitable (caffeine/nicotine)

- quicker than SA node

- premature contracts --> extra systole (= contraction)

- PAC (premature atrial contractions)

- PVC (premature ventricular contractions) --> more problematic

ectopic focus

- abnormal pacemaker

- may appear and take over pacing of heart rate

systole

contraction

diastole

relaxation

cardiac cycle

- 72 bpm, complete cycle is 0.8 seconds

1. atrial and ventricular diastole

- atria and ventricles relax SIMULTANEOUSLY, blood enters atria and ventricles

- ventricles fill with blood

- get 70% of what will be end diastolic volume (EDV)

2. atrial systole (contraction)

- atria contract while ventricles are still relaxed --> push blood through AV valves to top off ventricles

- bicuspid and tricuspid open to give final 30% of EDV

- top off ventricles (still in diastole) --> total EDV is 120-130 mLs (one ventricle)

3. atria relax while ventricles contract (push blood out of ventricles through semilunar valves)

- ventricular contraction from apex up cause blood to go upwards

- blocked from atria by AV valves tethered to chordae tendinae attached to papillary muscles (ventricles)

- blood hitting AV valves as they close --> first heart sound, "lub"

- starts first isovolumetric phase

- pressure builds in ventricles --> semilunar valves open

- amount of blood out = stroke volume (70-90 mL per ventricle)

- semilunar valves close --> second heart sound "dub", starts second isovolumetric phase

- EDV-SV = end systolic volume (ESV)

- AV valves open

4. atria and ventricles relax simultaneously

end diastolic volume (EDV)

- volume of blood in each ventricle at end of ventricular diastole

- 70% from atrial and ventricular diastole (step 1 cardiac cycle)

- 30% from atrial systole (step 2 cardiac cycle)

- total EDV is 120-130 mL (one ventricle)

lub (first heart sound)

- sound caused by closure of the atrioventricular valves

- during ventricular systole

- starts first isovolumetric phase

dub (second heart sound)

- sound caused by closure of semilunar valves

- during ventricular systole

- stats second isovolumetric phase

end systolic volume (ESV)

volume of blood remaining in each ventricle after systole

dicrotic notch

- aortic semilunar valve closes at end of ventricular systole

- marks beginning of ventricular diastole

electrocardiogram (ecg)

- 12 leads placed at various points on body

- 3 are bipolar --> voltage difference between arms or arm and leg

- 9 are unipolar (6 chest leads)

- 12 different tracings comparing with another and normal records to determine if:

1. conduction pathway is abnormal

2. heart is enlarged

3. certain regions are damaged

larger p wave

indicate enlargement of atria

enlarged Q wave

may indicate heart attack

enlarged R wave

enlarged ventricles

flat t wave

not getting enough O2 (coronary artery disease)

elevated t wave

hyperkalemia

long p-q interval

- conduction time between beginning of atrial and ventricular contractions

- if there is scar tissue because of coronary artery disease or rheumatic fever --> signal have to go around damaged tissue --> takes longer --> uncoordinated contractions