the cells that coordinate

    the contractions 

the contractions 

called the 

wall of right atrium

SA node – sinoatrial node

junction between right atrium and right ventricle

AV node – atrioventricular node

conducting cells

throughout myocardium

in AV bundle

in bundle branches

in Purkinje fibers

most of these conducting cells are smaller than the working contractile cells

and those in the nodes are UNSTABLE

they cannot maintain a STABLE resting potential

so these cardiac muscle fibers are SELF-EXCITABLE

they depolarize spontaneously and cause those nearby to also depolarize

is a gradual depolarization

slow inflow of sodium ions

no outflow of potassium

SA 

80-100 / minute

parasympathetic system – vagus nerve

– these begin and distribute the impulses

Initiate action potentials 

these are only a small percentage of the heart cel

your personal pacemaker

sends out an action potential which reaches the AV node in a fraction of a second

message sent along internodal pathways – see yellow lines

BUT – stimulus is also passed to the muscle cells of both atria

so both atria contract

stimulus only reaches throughout the atria

ventricles do not feel the stimulus

these cells are smaller than the cells that conducted the impulse here from the SA node

so impulse SLOWS

impulse is delayed here

allows atria time to finish contracting

230 bpm higher than that is abnormal state and movement of blood through the pump is dangerously reduced

damage this and ventricles don’t get the message

radiate from apex toward the base (top) of heart

cause ventricles to contract in a rhythmic wave from inferior to superior aspect

pushing blood toward the exit vessels

SO BOTH VENTRICLES CONTRACT AT ABOUT THE SAME TIME

then the heart rests

= damage to any part of this conduction pathway

could slow it down or cause timing disruptions

ECG is used to diagnose

= INTRINSIC

DOES NOT NEED THE NERVOUS SYSTEM

in the heart muscle –

the action potential  lasts much longer (250ms +)

compare to skeletal muscle = (1 -2ms)

so the duration  of contraction is also much longer compared to skeletal muscle 

prevents – fast and ineffective contractions which would make the ‘pump’ useless

–nearby cell has just passed on an impulse

sodium channels open and sodium rushes into cell

this depolarizes the membrane

channels quickly close

the plateau

as sodium channels are closing – calcium channels (slow channels) open slowly and stay open a relatively long time

so the transmembrane (across the membrane) potential remains near 0mV for awhile

THIS IS THE MAJOR DIFFERENCE BETWEEN THE ACTION POTENTIAL IN SKELETAL MJSCLE AND CARDIAC MUSCLE

transmembrane potential drops below 0

note green line starting back down

cell begins throwing sodium out BUT…

calcium channels open (slow calcium channels)

so the loss of  positive sodium is balanced by the gain of positive calcium  (2)

accounts for the slow downward trend of the mV line

finally the calcium channels begin to close

now the slow potassium channels begin opening (3)

potassium rushes out of cell

now cell must rearrange ions to suit

THIS LIMITS HEART RATE

inside the myocyte  in ventricle = -90mV

when nearby cells stimulated = starts to lose ions and becomes -75mV

that is threshold and impulse proceeds

rapidly sodium influxes and depolarization occurs

note straight green line from 4 to 1

the line is above the 0 mark = depolarization ( reversal of charge) 

sodium channels close quickly

and sodium is pumped out of the cell

depolarization when sodium enters

this also opens channels for calcium to enter

once inside the calcium ions stimulate the SR to release the rest of the calcium (slow calcium channels)

so the depolarization wave moves down the T tubules to the SR

next sodium is no longer entering and is being pumped out

the depolarization is briefly prolonged by the calcium

this is the PLATEAU

potassium is pumped out to repolarize the membrane

then the pumps rearrange the ions…..

recall that the calcium entered during plateau

the entering calcium was about 20% of that required for contraction

but its arrival triggers the rest to be released from the sarcoplasmic reticulum

THIS IS ANOTHER REASON WHY CALCIUM IS SO IMPORTANT  AND SO TIGHTLY REGULATED

calcium channel blockers (verapamil) decrease the contractility of the heart  (BP med)

there are more mitochondria in cardiac muscle than in skeletal muscle

cardiac muscle uses aerobic respiration

anaerobic metabolism (ischemic condition) would produce too much acid, which hinders ATP production

gap junctions would close and isolate the damaged cells

heart uses glucose and fatty acids

also uses lactic acid from skeletal muscle

has a reserve of oxygen in myoglobin

Remember – atria go through systole and diastole then the ventricles go through systole and diastole

Remember – atria go through systole and diastole then the ventricles go through systole and diastole

heart is in total relaxation

heart blood pressure is low as blood enters atria and flows into ventricles (passively)

AV valves are open, 

atria contract and squeeze blood

THIS pushes rest of blood into ventricles – fills them up

now the ventricles are filled – called END DIASTOLIC VOLUME (EDV)  - lots of blood in ventricles now

Ventricular systole - 2

Atria relax (diastole for atria) 

Rising ventricular pressure (contraction)results in closing of AV valves (blood pushes back against valves)

called isovolumetric contraction

ventricles are starting to squeeze out the contained blood, but no valves are open yet

Ventricular ejection phase opens the semilunar valves (when ventricles squeeze – blood has nowhere to go but out through the SL valves)

Early diastole

Ventricles relax -3

Backflow of blood in aorta and pulmonary trunk has closed semilunar valves

remember - some blood remains in the ventricles

called END SYSTOLIC VOLUME (ESV)

ABOUT 40% OF BLOOD STILL IN HEART

what has been squeezed out = EJECTION FRACTION

blood flow through the heart is controlled by pressure changes

blood flows down its pressure gradient

pushes through any weaker opening

the pressure changes are caused by the contraction and relaxation of the myocardium

the ventricles fill mostly by passive flow of blood – explains why damage to atria is survivable, while ventricular damage is life-threatening

blood flow through the heart is controlled by pressure changes

blood flows down its pressure gradient

pushes through any weaker opening

the pressure changes are caused by the contraction and relaxation of the myocardium

the ventricles fill mostly by passive flow of blood – explains why damage to atria is survivable, while ventricular damage is life-threatening

the autonomic stimulation, slowing heart rate and causing vagal tone

vagus – puts the brakes on

norepinephrine

more calcium enters which increases CONTRACTILITY

glucagon, thyroxine, digitalis also enhance contractility

tells us how much per squeeze

Lots of factors come into play here

preload

afterload

ability to contract – contractility

blood waiting to be pumped out of the ventricle

how much might this be????

how long did the ventricle have to fill up?

THE FASTER THE HEART - BEAT THE SHORTER THE AVAILABLE FILLING TIME

how fast was the blood moving from the atrium to the ventricle

how fast was it coming back from all over the body?

this is the blood that didn’t make it out during the contraction

remember – there is some blood left behind

THE STROKE VOLUME HAS BEEN EJECTED

How much managed to exit the heart, leaving behind the ESV??

what was the preload?

how well did the ventricle squeeze?

what was the afterload?

Preload – amount ventricles are stretched by contained blood 

affects end diastolic (relaxation) volume – how much blood is in ventricle at end of relaxation phase

greater the EDV (end diastolic volume)-   the larger the preload (of blood)

when you are at rest = your EDV is comparatively LOW

you’re not stretching your ventricles much

if you exercise = EDV increases and myocardium stretches further – more blood pumped out of heart

this is how much blood is ready to go before the ventricles contract

more in = more out

Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume

Law – ‘more in = more out’

stretch the ventricular muscle = it contracts harder

Exercise increases venous return to the heart, increasing SV (because preload is more)

but too much = ventricle can’t pump well =CHF

Blood loss and extremely rapid heartbeat will decrease SV=preload is less

Ex. -not much blood entering and heart will increase pace to try to keep up the pressure – but output will be less

Contractility – cardiac cell contractile force due to factors other than EDV

Ex. Calcium, thyroxine, epinephrine, digitalis-increase

results in more blood ejected from heart

Ex. damaged heart = decreased contractility = stroke volume down

Afterload – back pressure exerted by blood in the large arteries leaving the heart

‘resistance in the pipes’ – What is in the way of blood leaving the heart?

clots, pulmonary edema = higher afterload

if increased afterload then stroke volume goes down

If HTN = ventricles don’t eject as much blood = more blood remains in heart = reduced stroke volume

Coronary atherosclerosis

Persistent high blood pressure

Multiple myocardial infarcts

Pulmonary problems

Valve problems

Congestive heart failure (CHF) is caused by:

small areas of the heart muscle are no longer coordinated with the rest of the muscles

blood is no longer effectively moved through the heart

heart rate under 60 beats / minute

in athletes = hypertrophy and SV is higher= resting heart rate can be lower and still provide same output

but in diseased patient = not enough blood delivery to the tissues

– more than 100 beats  minute

which way does stoke volume go?

down because no time to fill

what happens to lung’s ability to exchange oxygen?

not enough time for RBCs to exchange

decrease the workload to allow repair

so give vasodilator and drugs to decrease heart rate

 treatment for a mild heart attack with no drop in arterial pressure

first priority is to maintain arterial pressure

give vasoconstrictor

 treatment for severe HA that shows rapidly dropping arterial pressure

Blood pressure

Resistance

Heart must push with enough pressure to overcome the resistance in the network

So the more pressure – the more flow

 BUT the more resistance – the LESS flow

There is a big pressure gradient between the aorta and the far capillaries

Various control centers will adjust the whole system

Referred to as peripheral resistance (PR)

Resistance – opposition to flow 

Measure of the amount of friction blood encounters

vessels themselves – length and diameter

thickness of blood - viscosity

flow rates across surfaces – are there eddies or turbulence?

So what might cause RESISTANCE?

the longer the vessel the more friction 

the farther the blood travels – the more resistance is encountered

Ex. adding pounds = need for more vessels = more peripheral resistance

friction occurs next to vessel wall

Ex. smaller the vessel the more resistance – larger vessels are not very resistant to blood flow

the blood near the center of the flow is not influenced by the sides of the vessel

how thick is your blood?

compare syrup to water as it flows

healthy person has stable viscosity

eddies and swirls

occurs in heart and larger vessels

not supposed to occur in smaller vessels - if so = damage

are the major determinants of peripheral resistance

Fatty plaques from atherosclerosis: 

Cause turbulent blood flow

Dramatically increase resistance due to turbulence

turbulence is not smooth flow

Resistance makes more of an impact on tissue perfusion

Vessels can dilate and feed a particular area especially well, without the rest of circulation being disturbed

The heart will still be pumping out the same amount of blood

but arterioles may provide MORE or LESS resistance – this has the most impact on resistance

Resistance makes more of an impact on tissue perfusion

Vessels can dilate and feed a particular area especially well, without the rest of circulation being disturbed

The heart will still be pumping out the same amount of blood

but arterioles may provide MORE or LESS resistance – this has the most impact on resistance

Is highest in the aorta

Declines throughout the length of the pathway

Is 0 mm Hg in the right atrium

20 to 40 mm Hg

Low capillary pressure is desirable because high BP would rupture fragile, thin-walled capillaries

Lower BP is still sufficient to force filtrate out into interstitial space and distribute nutrients, gases, and hormones between blood and tissues

20 mm Hg 

A cut vein has even blood flow; a lacerated artery flows in spurts

Venous return in the larger vessels offers less resistance and the blood flow increases

Cooperation of the heart, blood vessels, and kidneys

Supervision of the brain

low, but determines amount of blood entering heart

veins become bigger closer to heart

less resistance

needs to overcome gravity

muscles compress

respiratory pump – rising pressure in thoracic cavity (exhalation) – pushes blood into the right atrium

works because of water pressure (hydrostatic)

solutes are moved as  solution flows past a membrane that allows them to pass through

works because of osmosis

osmotic pressure of a solution = how many solutes contribute to the attraction of water

blood colloid osmotic pressure or oncotic pressure

REMEMBER – solutes attract water – it wants to move toward the solutes to even out its own gradient

net hydrostatic pressure =

add up the amount of force driving fluids out of blood (Ex. 35 mm Hg)

plus the amount of force of the fluid pushing back against the capillary (Ex. small, negligible value)

net colloid osmotic pressure

add the attractive force (proteins) in the capillaries  to ‘lure’ water back into the capillary

plus the attractive force of the very few proteins in the nearby tissues (Ex. also negligible)

net hydrostatic pressure + net colloid osmotic pressure

blood flows faster in that area

histamine dilates blood vessels

lactic acid from exercise

rising levels of hydrogen (pH is moving toward acid)

temperatures increase in that area

causes smooth muscles of precapillary sphincter to relax

sphincters tighten

wounds – platelets and other chemicals cause vasoconstriction

cold

cardiovascular center

acceleratory part increases your cardiac output with sympathetic messages

inhibitory center uses the parasympathetic

– produce VASOMOTOR TONE

keeps arterioles a bit constricted

with small adjustments to arterioles – blood pressure (peripheral resistance) is controlled

Pressure Receptors called BARORECEPTORS

sense the amount of stretch in various organs

in CV system – located

near internal carotid arteries (carotid sinus)

in wall of ascending aorta

in wall of right atrium

parasympathetic nerves put the brakes on (Ach)

vasomotor center dilates vessels

what happens if pressure is sensed as too high?

sympathetic nerves stimulate heart (EP)

sympathetic neurons constrict vessels

what happens if pressure is sensed as too low?

Valsalva's maneuver

vena cava collapse, return to heart decreases

drop in CO and BP

aortic and carotid baroreceptors notice

heart rate increases and blood vessels constrict

release the pressure and heart returns to normal

but there will be a moment of high blood pressure

sensory receptors notice changes in your carbon dioxide, oxygen, or pH levels

in blood AND CSF

these are specialized cells near the carotid sinus and in the aorta (carotid body, aortic body)

if a rise in carbon dioxide (or a fall in pH)

these sensory cells notice  (cardiac center is stimulated)

so heart rate goes up, bv constrict (BP goes up) =blood pressure rises

causes intense vasoconstriction in cases of extremely low BP – saves water from exiting the body as urine

from pituitary

increase blood volume and BP

Direct renal mechanism

 alters blood volume by working faster to eliminate water (thus more urine)

involves the renin-angiotensin mechanism

special cells in kidney sense a fall in BP, release renin, which ultimately…

gets aldosterone into the system to save sodium

makes you thirsty

stimulates ADH secretion to save water in collecting ducts

stimulates heart and constricts arterioles

Blood pressure cycles over a 24-hour period

BP peaks in the morning (due to waxing and waning levels of retinoic acid)

Extrinsic factors such as age, sex, weight, race, mood, posture, socioeconomic status, and physical activity may also cause BP to var

condition of sustained elevated arterial pressure of 140/90 or higher

Transient elevations are normal and can be caused by fever, physical exertion, and emotional upset

Chronic elevation is a major cause of heart failure, vascular disease, renal failure, and stroke

important sign of circulatory shock

Threat to patients undergoing surgery and those in intensive care units

Delivery of oxygen and nutrients to, and removal of wastes from, tissue cells 

Gas exchange in the lungs

Absorption of nutrients from the digestive tract

Urine formation by the k

As temperature rises (e.g., heat exposure, fever, vigorous exercise):

Hypothalamic signals reduce vasomotor stimulation of the skin vessels-loosen the muscles

Heat radiates from the skin 

As temperature decreases, blood is shunted to deeper, more vital organs

Blood flow in the pulmonary circulation is unusual in that:

It’s a quick trip through the lungs 

Arteries/arterioles are more like veins/venules (thin-walled, with large lumens)

Vessels are so thin that it doesn’t take much pressure to move blood through

Vessels will constrict in areas of lung where the alveoli are blocked…..

any condition in which blood vessels are inadequately filled and blood cannot circulate normally 

Not enough blood flow to meet tissue needs

poor circulation resulting from extreme vasodilation

anaphylaxis or septic shock

So - in loss of blood volume and pressure (hemorrhaging) = less pressure forcing water and solutes out into tissues

so reabsorption dominates

= more fluids back to blood

Other factors in cardiovascular problems - - - -

in dehydration – the concentration of those large plasma proteins increases = calling more water back into blood

BUT --if liver damage - not enough of those large plasma proteins to lure the water back to blood

person has ascites