Download Anatomy and Physiology

Anatomy and Physiology
Cardiovascular Physiology
Hematocrit
- represents the percentage (%) of formed elements (all of the blood cells) in a 100cc
sample of blood
- Normal Hematocrit – 45% made up of formed elements, 55% is plasma
Vascular System
**Osmotic Pressure
- directly related to the concentration of non-diffusable solutes
- areas with high osmotic pressure draw water TOWARDS them
Proteins are the non-diffusable solutes (stuck)
- can’t leave the vascular system, stuck inside
- responsible for the osmotic pressure
- draw fluids in (not all of it) – lymphatic system takes care of the balance
Vascular System - conduit, or system of tubes, for the distribution of oxygen rich blood
to the capillaries and for the return of oxygen deficient blood to the heart
In carrying out this task (serving as a conduit), in the process of doing it, it performs
several other functions
Among them are:
1 - vascular system buffers pulsatile input from the heart and produces a steady
capillary flow
2 - helps to regulate volume and pressure in various segments of the vascular tree
3 - maintain a continuity of circulation, while at the same time, permitting free
interchange between vascular and extravascular compartments in the capillary beds
Endothelial lining
- continuous, no break
Smooth muscle
- under control of ANS
L/R coronary arteries the only vessels to come off ascending aorta and arise behind the
cusps of the aortic semi lunar valves. When the left ventricle is in systole and blood is
exiting the left ventricle thru semilunar aortic valve, so valve is open, however at that
moment the openings to the coronary arteries are closed, they are blocked by the aortic
valve. Only when LV is in diastole (relaxed), that the coronary arteries are perfused with
blood.
Great vessel – one that directly enters or leaves the heart
Pulmonary arteries – NOT a great vessel
Pulmonary trunk – IS a great vessel
Right half – pulmonary circuit
Left half – systemic circuit
Blood Flow
Superior and Inferior Vena Cava  Right Atrium  Tricuspid Valve  Right Ventricle
 Pulmonary Semilunar Valve  Pulmonary Trunk  Right and Left Pulmonary
Arteries  Lungs  4 Pulmonary Veins  Left Atrium (4 pulmonary veins enter
here) Bicuspid Valve  Left Ventricle  Aortic Semilunar Valve  Aorta  System
There is a fibrous skeleton, made of collagen fibers, that electrically isolates the
chambers from each other so if problem arise in one chamber will not affect another. It
also gives shape and reinforcement to the heart.
There are NO VALVES between the veins that feed the atria and the atria themselves
- flow into chambers is based on pressure ONLY. When pressure in veins is
greater than the left atrium blood will flow in. (pulmonary edema- blood doesn't flow into
LA readily and backs up in valve or back to lung.
Electrical conduction: start with SA node, which has an intrinsic rhythm of depolarizing
one time every 8 tenths of a second, is what is responsible for a resting heart rate of 72
BPM. (60 sec divided by 0.8 = 72 BPM). fibrous discharge prevents electrical impulse
from going anywhere, so fibers in the inter atrial septum will conduct message to the left
side of the heart. B/c of the histology of the heart of cardiac muscle, message is sent thru
heart very rapidly. In RA, near the septum, is the AV node receives the electrical signal
from the SA node, when message received, it holds message momentarily, and then
releases into the Bundle of His, this then divides into R/L bundle branches. left further
divides into two smaller branches because left ventricle is larger. They surround heart
giving off purkinje fibers on both sides, helps with depolarizing electrical charge around
heart.
Valve – one way flow
Sphincter – ring of muscle tissue; can flow in either direction
Epicardium – outer
Myocardium – middle
Endocardium – inner
Wall of left ventricle AND myocardium – 4-5x times thicker because the right ventricle
is pumping blood only to the lung (low pressure system)
- left ventricle is pumping blood all over the body – needs to develop more
pressure
Vascular sys serves as a conduit (sys of tubes) for the distribution for o2 rich
blood to the capillaries and for the return of O2 def blood to the heart. In carrying out this
task of serving as a conduit, it performs several other functions, among them are:
The vascular sys buffers pulsatile input from the heart and produces a steady capillary
flow
Helps to regulate volume and pressure in varies segments in the vascular tree
Said to maintain a continuity of circulation while at the same time free interchange betw
vascular and extravascular compartments in the capillary beds
The heart embryonically started as two blood vessels thus the similarities in the linings
Tunica interna: smooth endothelial lining, continuous with inner lining of the heart
Tunica media: is where the muscle is
Tunica externa: tough outer sheath
Capillary heart is the exchange vessels
Arteries are classified based on function: as elastic (the largest and closest to the heart),
muscular (as they go away from heart, less elastin and more smooth muscle), and then to
distributing (as smooth muscle decreases)
Great vessels –directly enters/leaves the heart
**Know the valves and the great vessels of the heart**
right half – sys circuit
left half – pulm circuit
Cardiac Muscle Tissue
Histology – basis on which heart functions (unique)
Like skeletal muscle tissue, Cardiac tissue is:
- striated
- contains actin and myosin (sarcomeres), as well as all the same contractile
proteins
- contracts according to the sliding filament theory of muscle contraction
Unlike skeletal muscle tissue:
-cardiac relies on extracellular CA to excite contractile process (skeletal stores Ca)
Cardiac muscle cells are:
- short
- branched
- interconnected
-Further adjacent cardiac muscle cells are separated from eachother by gap junctions
(intercalated discs)
- have an electrical resistance that is 1/400 (400 times less) the resistance that
exists between cells not joined by gap junctions
- as a result of the structure and these gap junctions, electrical signals that
originate at any point in the mass of myocardial cells spreads VERY rapidly to all other
cells at the mass of cells that are interconnected
- as a result, cardiac muscle functions as if it were ONE LARGE
MOTOR UNIT, even though there are NO motor units actually in cardiac muscle.
(can change BPM by increasing force of contraction, but if no motor units, how can
increase force of contraction? length tension relationship: enough actin length to bind and
contract. In cardiac muscle, the sarcomere is much shorter (everything squished together)
and more overlapping of actin and myosin. also why with increased volume (EDV-end
diastolic volume) cause increased contraction because stretch out sarcomere and have
more to come back to resting.
- there are NO graded contractions in cardiac muscle
Functional syncytium – often used to describe myocardial contraction (functions as if
one large cell, because of unique histology)
All areas of the heart are capable of generating an electrical signal (auto rhythmic)
- but the various areas of the heart do this at different rates
- The SA node (in right atrium)
- spontaneously active every 8/10 of a second
- functions as the heart’s pacemaker
As you descend:
- Atrial tissue is spontaneously active 60 times a minute
- The AV node – 40 times a minute
- Ventricular tissue – 20 times a minute
(as you get deeper into the heart, the activity decreases)
All areas of the heart are spontaneously active
The area of the heart that is spontaneously active at the fastest rate assumes the role of the
pacemaker (SA node)
Cardiac tissue AND the SA node possesses a pacemaker potential
- exists in excitable tissue (nerve, muscle) with NO resting membrane potential
- the cells of the heart, both the nodal (electrical) system and the muscle system,
-Do NOT possess a resting membrane potential because these cells lack the ability
to keep Na+ ions out
- allows Na+ to go in, causing it to become more positive towards firing potential,
firing action potentials spontaneously – no stimulus involved (autorhythmic).
producing spontaneous depolarization and heart beat. All cells in heart do this but
SA node does this the fastest.
Electrophysiology of Cardiac Muscle Tissue
- Action potential in cardiac muscle rises from about -80 to about +20 - +30 millivolts
(inside compared to outside)
- when it reaches that point, it then exhibits a plateau that lasts in ventricular
muscle for about 3/10 of a second (.25-.3 sec)
- then gets a rapid repolarization
- The presence of that plateau in the action potential causes the muscle contraction to last
20-50x times longer in cardiac muscle than in skeletal muscle
Two major differences between cardiac and skeletal that result in this plateau, and
responsible for the prolonged muscle contraction
1- Presence of slow Ca+/Na+ channels in cardiac muscle
Skeletal Muscle
- Action potential of skeletal muscle is due almost entirely to the SUDDEN, RAPID
opening of fast Na+ channels that allow tremendous amounts of Na+ to enter the muscle
fiber
- these channels remain open for only a few 10 thousandths of a second
- then rapidly close
- repolarization occurs
- action potential is over
Cardiac Muscle
- Action potential is caused by two types of channels being opened.
A- same fast Na+ channels that exist in skeletal muscle; quickly start to close
(why
there is a dip in the action potential graph)
B- slow Ca+/Na+ channels
- open a little bit later, but remain open for several tenths of a second
- large amount of Ca+ ions (major) and Na+ ions continue to rush into the
cell, prolonging the depolarization
- this is what causes the plateau in cardiac muscle action potential
- Ca+ ions excite the contractile process (move the troponin and
tropomyosin – allow cross bridges to interact with the actin) [allows the
sarcomeres to work]
2- Immediately after the onset of the action potential in cardiac muscle, the permeability
of the cardiac muscle cells membrane to potassium decreases about 5 fold
- prevents the outflow of potassium (traps it inside the cells)
- occurs during the plateau when the slow Ca+ channels are open
- prevents early repolarization
After about .25-.3 second, when the slow calcium channels close, the membrane’s
permeability for potassium returns to normal
- the membrane’s potential returns to its resting level
Refractory Period
- period of time when excitable tissue (muscle, nerve) will NOT respond to another
stimulus
Absolute Refractory Period
- period of time when no matter what you do, the excitable tissue WON’T respond
Relative Refractory Period
- period of time in which a stronger than normal stimulus WILL cause a response. when
membrane potential below zero and headed back towards -80. There is relative in
ventricular tissue which is about 0.5 seconds.
The absolute refractory period of ventricular tissue is .25-.3 seconds, which is exactly
equal to the duration of the action potential (period of time when it’s absolutely
refractory) b/c of the Ca channels and the plateau.
- THEREFORE, you cannot get this in cardiac muscle, preventing tetany
- will not get stimulated by anything until it is totally relaxed
Short Refractory Period
- less than .05
- during this period, that people with electrolyte imbalances or problems with their
conduction system  arrhythmia to occur
Terms
Aneurysm – an insult to an artery – ballooning out of an artery wall, making that spot
weaker
- Triple A’s – Abdominal Aortic Aneurysm – if it ruptures, no time to get to
hospital
Hemorrhoid – typically associated with rectal veins – venous problem – a type of
varicosity (balloons outward)
Arteriosclerosis – describes several different disease processes – general condition in
problem of arteries
Atherosclerosis – accumulation of plaque or fat on the wall of the artery (one type of
arteriosclerosis)
Cardiac Cycle
- refers to a repeating pattern (cycle) of contraction or systole (contraction) and diastole
(relaxation)
Consists of:
- electrical, mechanical, and acoustical events (ORDER IS CRITICAL – describes the
sequence in which they occur)
- electrical always proceeds mechanical
Atrial systole occurs during ventricular diastole (be careful not to confuse systole with
depolarization)
Ventricular systole occurs during atrial diastole
Upper and lower chambers CANNOT be in systole at the same time
- CAN both be in diastole at the same time
- The left and right atria contract simultaneously followed in about .1-.2 seconds by the
contraction of the left and right ventricle
- During atrial and ventricular diastole (relaxed), venous return of blood fills the atria and
because the AV valves are open, fills the ventricles
- It has been measured that the ventricles are 80% filled with blood before the atria
contract
- Then contraction of the atria provide the final 20% to the ventricle
- The volume of blood at this point at the ventricles is called End
Diastolic Volume (E.D.V.) – volume of blood in ventricles at the end of ventricular
diastole
- Contraction of the ventricles ejects about 2/3 of the blood of EDV in the ventricles (at
rest) leaving behind the End Systolic Volume (E.S.V.) – volume of blood in ventricles at
the end of ventricular systole
Stroke Volume (SV) – amount of blood ejected from the ventricle per beat
(mathematical difference between EDV and ESV between each beat.
EDV – ESV = SV
100ml – 33ml = 67ml
Ejection Fraction (stroke volume expressed as a percent) 67/100 = 67% (normal is about
65-66 percent)
Often represented as a percent
- when expressed as a percent, it is referred to as an Ejection Fraction
At an average heart rate of 72 beats per min, each cardiac cycle last .8 of a second
- at rest, of those 8/10 of a second, the heart is in diastole for .5 and systole for .3
When left ventricle is in diastole, the average pressure in the systemic arteries is
80mmHg
**LOOK AT BOOK FOR CARDIAC CYCLE**
START of CARDIAC CYCLE
EDV in Left ventricle in diastole – contains its end diastolic volume, ventricles now
loaded with EDV. This is the start of cycle.
Phase 1 - Isovolumetric Contraction
- left ventricle contracts (blood not moving yet though)– pressure in left ventricle
exceeds left atria AV valve closes
- pressure in aorta exceeds pressure in ventricle  semilunar valve closes
- the AV valve and the semilunar valve are closed
- all valves are closed
- volume isn’t changing
Valve open and close based on pressure:
When pressure above the valve is higher than the pressure below  valve opens
When the pressure below the valve is higher than the pressure above it  valve closes
Cordae tendonae – protect valves from prolapsing
As soon as pressure in ventricle exceeds the pressure in the aorta, we enter Phase 2
(Ejection)
Phase 2 - Ejection
Begins as soon as pressure in ventricle exceeds pressure in the aorta:
- the semilunar valve opens and pressure is ejected
During ejection, the pressure in the left ventricle reaches 120mmHg (Right = 25mmHg)
even while the ventricular volume decreases (even with blood leaving)
Phase 3
- starts as Pressure in the ventricle starts to fall and back pressure from the aorta closes
the aortic semilunar valve
- Pressure in the aorta falls to 80mmHg
- Pressure in the left ventricle falls down to 0
Phase 4 – Isovolumetric Relaxation
- the AV valve and the semilunar valve are closed because:
- pressure in ventricle is higher than pressure in atria
- pressure in aorta is higher than pressure in ventricle
- Lasts only till ventricular pressure falls below atrial pressure
- when ventricular pressure is less than the atrial pressure  valve opens
Phase 5 – Rapid Filling
- venous return is filling the atria and blood is falling through the open AV valves into the
ventricles
Phase 6 – Atrial Systole
- adds the final squirt of blood to the ventricles
- volume of ventricles are at E.D.V (End Diastolic Volume) – ready for next
isovolumetric contraction, and all phases to begin again
Basic EKG (electrical before mechanical)
P Wave – represents atrial depolarization (followed by atrial systole)
QRS Complex – ventricular depolarization / atrial re-polarization (larger b/c ventricular
muscle is larger (followed by mechanical ventricular systole)
T Wave – ventricular re-polarization (followed by mechanical ventricular diastole.
**ST segment: critical, end of s and beginning of T is when ventricles are contracting.
Ischemic attack will cause change in ST segment. (in normal heart, line thru waves, to
return, is usually isoelectric, same)
Atrial repolarization occurs at the same time the ventricular depolarization
If there is no electrical depolarization, there is no muscle contraction
Five Things That Can Be Determined By EKG
Heart Rate
Heart Rhythm
Axis of the Heart (position of heart in the thorax)
Hypertrophy (enlargement- difference between clinical-wall thinner, heart bigger and
athletes- wall thicker)
Infarct (dead tissue)- flat line
Heart Sounds
1- Lubb
- caused by closing of the AV valves
- associated with ventricular systole (contracting)
ALL HEART SOUNDS ARE CAUSED BY CLOSING OF VALVES
2- Dubb
- closing of the semilunar valve
- associated with ventricular diastole (relaxing)
Dicrotic Notch – a notch turbulence (a brief change in pressure) when the aortic valve
closes
3- Murmur (graded on grade 1-6, one minor, 6 major)
- abnormal heart sound
Two Categories:
A- Stenosis
- occurs when the valve doesn’t open properly
B- Regurgitation
- occurs when the valve doesn’t close properly
- grades on a series of 1 (almost benign) to 6 (serious)
SA node (right atrium)  Left Atria
AV node (right atrium)  Bundle of His  Bundle Branches (left [splits into two] and
right)  Purkinje Fibers – distribute electrical message
AV node, during the cardiac cycle, stalls the cardiac message (holds is back for tenths of
a second) – acts as a resistor
- to give the atria time to contract and eject blood to the ventricles
Cardiac Ouput (in ml/min)
**Cardiac Output = Stroke Volume (beats/min) x Heart Rate (ml/beat)**
Average heart rate of 70-72 beats per min
Average stroke volume – 70-80 ml/beat
Average cardiac output – 5000 ml/min
5000ml/min ~ 70-72 beats/min x 70-80 ml/beat
**Any change (increase or decrease) in cardiac output must be accompanied by a change
in either heart rate and/or stroke volume**
Regulating Heart Rate
- if left alone, then the heart will contract due to the autorhythmicity of the SA node - will
keep it beating
Normally the heart is continually under the influence of the ANS (Autonomic nervous
system) If cut this connection, heart will still beat b/c it doesn't need any outside
influence to beat.
Norepinephrine and Epinephrine
Norepinephrine (primary neurotransmitter in sympathetic divison), released primarily by
symphathetic nerve endings and epinephrine, from the adrenal medulla, are both positive
chronotrophs or chronotropic agents (increase heart rate)
These agents:
INCREASE the rate of diastolic repolarization
INCREASE cardiac rate by increasing the rate of the SA node
INCREASE the speed of conduction through the AV node
Overall, they effect the way the heart beats (affects heart rate)
 Increase heart rate
These agents also have an effect on stroke volume
- positive inotropic agents – increase the strength of atrial contraction AND
increase the strength of ventricular contraction
 Increase stroke volume
Acetylcholine (Ach)
- primary neurotransmitter of the parasympathetic nervous system
- hyperpolarizes the SA node (further away from the threshold)
- DECREASE the rate at which it fires
- DECREASES the rate of conduction through the AV node
- DECREASES the rate of diastolic repolarization (opposite of epinephrine)
- negative chronotropic agent – decreases heart rate
- DECREASES the strength of atrial contraction
- NO affect on the strength of ventricular contration
Increase heart rate by: Increase sympathetic tone or decrease parasympathetic tone or
have a mixture of both, which is usually what happens
Stroke Volume
- regulated by EDV (End Diastolic Volume)
- frequently referred to as preload – load that ventricle has to work on when it
starts to contract
- SV is directly proportional to the preload (EDV)
- SV is directly proportional to contractility
- increase strength of contract, increase stroke volume (more will be pumped out)
- under the regulation of the mean (average) arterial pressure
- In order to eject blood, the pressure generated by the ventricles must be GREATER than
the mean arterial pressure (pressure in the aorta)
- The pressure in the aorta is referred to as an afterload - pressure imposed on the
ventricle after they begin to contract
Preload – volume of blood
Afterload – pressure in the aorta (important to cardiac function)
- Stroke volume is inversely proportional to afterload
- the higher the afterload, the lower the stroke volume
Blood Pressure
- the force against the wall of the vessel
As vessels lose elasticity, pressure inside them increases (analogous to vasoconstriction)
Frank Starling Law of the Heart
- as you increase EDV, you increase stroke volume
- associated with histology of sarcomere in cardiac muscle
Sarcomere
- from z line to z line, with thin filaments coming out from side and thick filaments in the
middle
- Zone of overlap – thick filaments overlap the thin filaments
In resting sarcomere of cardiac muscle:
- z lines are closer together
- zone of overlap is much greater
- by increasing EDV, you have ability to stretch it out and still have a zone of overlap
without separating the thin and thick filaments – more distance to contract
- if it contracts more, the more force it will have
Venous Return
Without venous return, there is NO cardiac output
Cardiac output and stroke volume are really controlled by factors associated with venous
return
Venous return is based on:
- total blood volume
- venous pressure
Mean Venous Pressure (average) = 2mmHg
- low, due to pressure drop
In venules (larger veins), the pressure is 10mmHg
The pressure where the SVC and the IVC come together and enter the right atrium, that
pressure is about 0 – ½ mmHg  the lowest
Pressure is venous system is lowest when blood enters the right atrium
Mechanisms to help ensure venous return
1- sympathetic stimulation of the veins
- when tunica media is stimulated  muscle contracts  vessel constricts 
elevating pressure to ensure venous return
2- skeletal muscle pump
- most veins run thorugh skeletal muscle
- tunica intima veins have valves – provide ONE way flow
- if pressure decreases, blood backs up – doesn’t pool
- squeeze muscle around vein and pushes blood up toward the heart
3- Pressure difference between the thorax and the abdomen that is a result of
ventilation or breathing
Coronary arteries come off ascending aorta right behind the flaps of the aorta semilunar
valve
- only arteries to come off ascending aorta (behind flaps of aortic semilunar valve)
During ventricular systole (left ventricle contracts):
- the flaps of the aortic semilunar valve are open, allowing blood to leave.
- at the same time, the coronary arteries are being blocked by that valve
- the coronary arteries are not being perfused with blood
During ventricular diastole:
- the flaps of the aortic semilunar vales are closed
- the coronary arteries are perfused
Hemodynamics (Physics of Blood Flow): flow dynamics
Flow=change in P/resistance
Flow is directly related to pressure
- indirectly related to resistance
F=changeP times pie times R to the fourth/8 L lambda
1/R= r to the 4th/ l lambda
R= l lambda (viscocity of fluid)/ r to the fourth
so,
The longer the vessel, the more resistance to flow
- Can’t change the length of a vessel
- Viscosity and radius change
Length of a Vessel
As the length of a vessel increases, resistance increases
As resistance increases, flow decreases
Viscosity
As viscosity increases, resistance increases
As resistance increases, flow decreases
Radius of Vessel
As radius increases, resistance decreases
As resistance decreases, flow INCREASES
Vasoregulate – change diameter or blood vessel (decrease or increase)
- vasodilation or vasoconstriction
**Vasoregulation is the single most powerful flow regulatory mechanism that your
body possesses
Vasoconstriction dramatically decreases flow
Without this regulation, you cannot function