CARDIOVASCULAR SYSTEM

The Heart
A. Circulatory circuits - blood flows between heart and peripheral tissues
1. Pulmonary circuit - carries blood to and from the gas exchange surfaces of
the lungs
2. Systemic circuit - transports blood to and from the rest of the body
B. Heart
1. Right atrium 2. Right ventricle 3. Left atrium 4. Left ventricle -

C. Blood vessels
1. arteries - carry blood away from heart (efferent vessels)
2. veins - carry blood toward the heart (afferent vessels)
3. capillaries - small vessels between the smallest arteries and veins; exchange
vessels

56

57

Heart Location & External Surface

A. Pericardial cavity - located in the mediastinum of the ventral cavity
1. Sits at oblique angle from ribs 2-5
2. Nestled between both lungs
3. Contained in protective/anchoring sac known as Pericardium
Pericardium: Double walled layer around the heart
A. Fibrous pericardium:
B. Parietal pericardium:
D.Visceral pericardium (epicardium) - covers
the external heart surface.
C. Pericardial cavity: Contains serous fluid to lubricate
membranes and allow for gliding
of one surface against another.
B. Heart Wall & Layers
D. Epicardium (visceral pericardium) - Most external.
E. Myocardium - cardiac muscle; forms the bulk of heart.
1. Connective tissue:
2. Annulus Fibrosus forms internal fibrocartalaginous tissue skeleton
for internal support and anchoring.
3. Internal skeletons role on containment of electrical signal
F. Endocardium - endothelium (simple squamous epithelium). Lines the
interior myocardium, continuous with blood vessels.

58

59

Myocardial Cell Structure

Similar structure to skeletal muscle in regards to striations, sarcomeres, sliding filament
theory. Different due to nature of continuous activity, speed needed for cardiac cycle,
endurance

1. Short, bunched/fat, tightly grouped structure

2. Interconnected via
a.
b.
c.
3. Large amount of mitochondria: Make up 25-35% of cardiac cell volume.
a.
b.
4. Contractile and pacemaker cells: Cardiomyocytes and autorhythmic respectively
5. Sarcomeres: Actin and Myosin filaments with respective bands
Interior Heart Anatomy
1. Right atrium - receives deoxygenated venous blood from the systemic circuit
a. Superior vena cava b. Inferior vena cava c. Coronary sinus 2. Right ventricle - receives deoxygenated blood from the right atrium
a. Tricuspid valve (right atrioventricular valve) - between right atrium and
ventricle:
1) chordae tendineae - small tendons attach to the 3 cusps
2) papillary muscles - projections in ventricle that anchor chordae
tendineae.
b. Interventricular septum - separates right and left ventricles
c.Pulmonary semilunar valve - has 3 thick semilunar cusps between right
ventricle and pulmonary trunk;
d. Pulmonary trunk - carries deoxygenated blood to the lungs via a split into
two arteries: the right pulmonary artery and left pulmonary artery.

60

3. Left atrium - receives oxygenated blood from the pulmonary circuit

a. Pulmonary veins (2) - from right lung and (2) - from left lung
4. Left ventricle - receives oxygenated blood from the left atrium
a. bicuspid valve (mitral valve) - between left atrium and ventricle:
1) chordae tendineae - small tendons attach to the 2 cusps
2) papillary muscles - function the same as in tricuspid valve
b. aortic semilunar valve - has 3 thick semilunar cusps between left ventricle
and ascending aorta; prevents backflow of blood into left ventricle.
5. Ascending aorta - carries oxygenated blood to aortic arch and descending aorta

61

Ventricular differences - Functional demand on right and left atria are similar, and
the two chambers look relatively the same, however demands on right and left
ventricles are very different, and the two have significant structural differences
a. Right ventricle - cavity is crescent-shaped and wraps around left ventricle.
a1.
a2.
b. Left ventricle - thicker wall (3 x thicker) than right ventricle and its cavity
is basically circular.
b1.
b2.

6. coronary blood vessels: Source of oxygenated blood to heart itself. Numerous

variability in branches off main coronary arteries
a. right coronary artery
1) atrial branches - to right
atrium
2) marginal branch - to right
ventricle
b. left coronary artery
1) atrial branches - to left
atrium
2) circumflex branch anastomoses with right coronary
artery
posteriorly
3) anterior interventricular
branch (left anterior descending
artery)

62

Heart Physiology
1. Conducting system: Intrinsic in nature. Does not require outside source to
"spark" action potential.
Sequence of steps in cardiac electrophysiology ( Setting the pace)
a. Sinoatrial (SA) node - cardiac pacemaker; fastest of nodal cells (80-100
beats/min.):
a1. Initial current spread via ______________ to atria and AV node
b. Atrioventricular (AV) node - AV node found in the floor of right atrium.
Delay in conduction from AV to rest of heart.
1.
2.
c. Conducting fibers - distribute
stimulus from nodes
c1. AV bundle (bundle of His):

c2. Right and Left bundle

branches - Continues along the
interventricular septum
before terminating into

c3.--> Purkinje fibers - fast

conducting cells that turn
"north" along ventricle walls.
More complex layout then
right due to size/function

63

Ionic movement in the intrinsic cardiac conduction system

This system consists of specialized non-contractile cardiac cells that "self-start" or initiate
the cardiac impulse and spread it through the specific conducting regions of the heart as
noted earlier

1. Post hyerpolarization, K+ channels close and slow Na+ channels open

2. Sodium influx brings membrane interior voltage to less negative state
3. At -40mv, Ca2+ channels open allowing rapid influx which cause the Action Potential
4. Ca2+ channels close and K+ channels open at end of AP which starts process of
repolarization.
5. K+ channels close once repolarization complete and process begins again with
opening of slow Ca2+ channels
A. Notice that the autorhythmic cells has NO stable resting membrane
B. Calcium drives the action potential rather than sodium

VS

64

65

Action Potential of Contractile Cardiac Muscle Cells

1. Fast voltage gated sodium channels open
which cause depolarization. These also close
quickly
2. This depolarization travels down TTubules which cause the SR to release Ca2+
The work on contraction then begins
3. Slow Ca2+ channels open in response to
extracelluar Ca2+ presence and they prolong
the AP

4. K+ channels are held in check briefly as

contraction completes
5. Slow Ca2+ channels finally close and K+ channels
open which begins process of repolarization
The Cardiac Cycle
Defined as all the events related to blood flow that occur during a single heartbeat.
Terminology of systole & diastole are associated with this cycle and bookend the events
of contraction and relaxation of the heart.

66

1. Low pressure both sides/top-bottom allowing blood to flow from atria to ventricle
a. AV valves open
b. Semilunar valves closed
c.
2. Ventricular systole
a. AV valves shut due to ventricular pressure
b. Semilunar valves still shut resulting in brief period of
3. Ventricular ejection
a. Pressure exceeds semilunar valves which force them open
4. Isovolumetric relaxation:
1. Early ventricular filling begins again
a. AV valves open (tricuspid and mitral valve)

Ventricular Function
Cardiac Output: Is known as the total volume of blood ejected from one ventricle in the
span of a minute. This can change in response to demand via Stroke volume, Heart rate,
or both.
Product of Stroke Volume (SV) x Heart Rate (HR).
SV= blood pumped out of one ventricle with each beat
Normal values: 75bpm x 70ml/beat= 5.25 liters per minute
Blood amount in normal adult: ~ 5 liters
1. Regulation of Stroke Volume
Difference in volume is determined by the amount of blood that was allowed to
fill the ventricles, and the amount remaining after ventricular contraction
Normal value is ~60% of blood in chamber is pumped out.
What then alters Stroke volume?
A. Preload: Degree to which cardiac muscles cells
are "loaded" with blood, which stretches the
sarcomeres and allows for stronger contraction via
maximum cross bridge formation
B. Contractility: The contractile strength achieved
at a given muscle length. Increased influx of
Calcium into cytoplasm from ECF and SR causes
increase in cross bridge binding which enhances
ventricular contractions
Sympathetic nervous system effects on calcium influx
67

C. Afterload: Pressure that must be overcome by the ventricles during

contraction to open the semilunar valves.
What then alters Heart Rate?
A. Autonomic Nervous System
1. Sympathetic system causes increase in HR via norepinephrine at
cardiac synapse.
2. Parasympathetic system uses acetylcholine to hyperpolarize membranes by
opening K+ channels.
*This is dominant resting system: SA node inherent rate vs. normal
resting HR
3. Atrial (Bainbridge reflex): Increased venous return to Atria causes stretch
reflex that signals SA node to make reflexive adjustments.
4. Baroreceptors(sense changes in blood pressure)and adjust autonomic system
for short term needs.

68

Heart Physiology
1. Conducting system: Intrinsic in nature. Does not require outside source to "spark" action
potential. FYI: If the heart is denervated surgically or due to medications, the heart rate will increase to roughly
100bpm in many cases. The resting HR we know as roughly 70bmp is due to parasympathetic influence of the SA
node

Sequence of steps in cardiac electrophysiology ( Setting the pace)

a. Sinoatrial (SA) node - cardiac pacemaker; fastest of nodal cells (80-100
beats/min.): Vagal Tone: The influence of the vagus nerve causes hyperpolarization of
the membranes by opening K+ channels. As we know this increases the permeability of the
membrane to K+ outflow and the cell interior becomes more negative which slows the rate of action potentials

a1. Initial current spread via gap junctions and internodal pathways to atria
and AV node. Internodal pathways are noncontractile cardiac cells that conduct impulses in
the heart

b. Atrioventricular (AV) node - AV node found in the floor of right atrium.

Delay in conduction from AV to rest of heart.
1. Why: Allows time for atria to contract and empty contents into
ventricles
2. How: Smaller diameter fibers and fewer gap junctions If the fibers are
smaller and there are fewer gap junctions, the signal bottlenecks so to speak and
the impulse is slowed. Much like merging onto a freeway during rush hour

c. Conducting fibers - distribute

stimulus from nodes
c1. AV bundle (bundle of His):
1. Only electrical connection
between atria and ventricles.
2. Very rapid conduction
There are no gap junctions between
atria and ventricle musculature. The
current must travel along the AV
bundle. This prevents irregular and
non-sequenced heart contractions.
The conduction speed must be rapid in
order to stimulate the ventricles to
contract in the right time and manner.

c2. Right and Left bundle

branches - Continues along the
interventricular septum
before terminating into
c3.--> Purkinje fibers - fast
conducting cells that turn
"north" along ventricle walls.
It is here that the wave of depolarization really kicks in for the ventricles. As the purkinje
fibers begin distal and move superior, the contraction follows the same path and the muscles contract in a manner
that forces the blood superior towards the semilunar valves. Ventricular muscle is stimulated by bundle branches
however speed of signal causes the bulk of the ventricular muscles to contract via Purkinje fibers. Repolarization
occurs in the opposite manner however it is not due to the conducting systems but that the cells activated last have
the shortest action potentials.

Ionic movement in the intrinsic cardiac conduction system

This system consists of specialized non-contractile cardiac cells that "self-start" or initiate the
cardiac impulse and spread it through the specific conducting regions of the heart as noted earlier

1. Post hyerpolarization, K+ channels close and slow Na+ channels open

Why post hyperpolarization? There is no stable resting membrane potential so the hyperpolarized state serves as a
start point. It is the opening of the Na+ channels that prevent a stable potential as we see by the graph

2. Sodium influx brings membrane interior voltage to less negative state

3. At -40mv, Ca2+ channels open allowing rapid influx which cause the Action Potential
4. Ca2+ channels close and K+ channels open at end of AP which starts process of
repolarization.
5. K+ channels close once repolarization complete and process begins again with
opening of slow Ca2+ channels
A. Notice that the autorhythmic cells has NO stable resting membrane
B. Calcium drives the action potential rather than sodium (see graphs below for comparison between
neural action potential and pacemaker action potential)

VS

Action Potential of Contractile Cardiac Muscle Cells

**know cycle**
1. Fast voltage gated sodium channels open
which cause depolarization. These also close
quickly
2. This depolarization travels down TTubules which cause the SR to release Ca2+
The work on contraction then begins
3. Slow Ca2+ channels open in response to
extracellular Ca2+ presence and they prolong
the AP Roughly 20% of calcium comes from
extracellular space. The remaining 80% is from the
sarcoplasmic reticulum. This is why we have an
additional step involved in calcium release at noted by
bullets 2 and 3. Bullet 2 is basis and bullet 3 (this one) has slightly more meat

4. K+ channels are held in check briefly as contraction completes

There are a small amount of K+ channels that remain open at this time however the voltage gated channels have not
yet opened to really drive the repolarization effect.

5. Slow Ca2+ channels finally close and K+ channels

open which begins process of repolarization

The Cardiac Cycle

Defined as all the events related to blood flow that occur during a single heartbeat.
Terminology of systole & diastole are associated with this cycle and bookend the events of
contraction and relaxation of the heart.

1. Low pressure both sides/top-bottom allowing blood to flow from atria to ventricle
a. AV valves open
b. Semilunar valves closed
c. Atria contract increasing pressure and ejecting more blood into ventricles
FYI: 80% of ventricular filling occurs prior to atrial contraction. The remaining 20% is post atrial contraction

2. Ventricular systole
a. AV valves shut due to ventricular pressure
b. Semilunar valves still shut resulting in brief period of isovolumetric contraction
Degree of pressure exerted on the semilunar valves from systemic circulation can obviously have an impact on the
amount of pressure is needed by the ventricles in order to force open the semilunar valves

3. Ventricular ejection
a. Pressure exceeds semilunar valves which force them open
4. Isovolumetric relaxation:
a. Pressure not great enough to open either the AV or semilunar valves in early diastole.
5. Early ventricular filling begins again
a. AV valves open (tricuspid and mitral valve)
Once pressure in atria in greater then ventricles, the valves open and passive filling begins again.

Ventricular Function
Cardiac Output: Is known as the total volume of blood ejected from one ventricle in the span of a
minute. This can change in response to demand via Stroke volume, Heart rate, or both.
Product of Stroke Volume (SV) x Heart Rate (HR).
SV= blood pumped out of one ventricle with each beat
Normal values: 75bpm x 70ml/beat= 5.25 liters per minute
Blood amount in normal adult: ~ 5 liters
1. Regulation of Stroke Volume
Difference in volume is determined by the amount of blood that was allowed to
fill the ventricles, and the amount remaining after ventricular contraction
Normal value is ~60% of blood in chamber is pumped out.
What then alters Stroke volume?
A. Preload: Degree to which cardiac muscles cells
are "loaded" with blood, which stretches the
sarcomeres and allows for stronger contraction via
maximum cross bridge formation
When thinking about preload we can imagine a load dropped onto a
trampoline. The greater the load, the more the trampoline should rebound.
We already understand the basics of muscle contraction strength in
skeletal muscle and optimal ranges of muscle length in order to allow for
more cross bridge formation. The cardiac muscle cells start in a
shortened range and then stretch with the influx of blood, which allows
for an increase in cross bridge formation and better contraction. Venous
return is the most important factor in stretching ventricles or creating end
diastolic volume (EDV). This can be caused by an increase in volume OR speed of venous return (Slow HR=more
filling time, or ,exercise shunts blood away from non crucial organs and muscle pump from activity increases
volume returned

B. Contractility: The contractile strength achieved at a given muscle length. Increased

influx of Calcium into cytoplasm from ECF and SR causes an increase in cross bridge
binding which enhances ventricular contractions
This is independent of EDV. Sympathetic nervous system innervates not only the conduction or
pacemaker system, but also influences the cardiac contractile cells via epinephrine (adrenal medulla) and norepinephrine (cardiac synapse) These hormones increase the calcium available for increased contractile
strength

C. Afterload: Pressure that must be overcome by the ventricles during

contraction to open the semilunar valves.
Not a major factor in health people. Roughly 80mm hg in aorta and 8mm hg in pulmonary trunk. With
hypertension the pressure can reduce the amount of blood ejected due to increased resistance at the valves

What then alters Heart Rate?

A. Autonomic Nervous System
1. Sympathetic system causes increase in HR via norepinephrine at
cardiac synapse. When physical or emotional stressors activate the SNS, the release of
norepinephrine (and epinephrine) binds to receptors on heart and causes threshold to be reached more quickly. The
pacemaker then responds with a faster rate.

2. Parasympathetic system uses acetylcholine to hyperpolarize membranes by

opening K+ channels.
*This is dominant resting system: SA node inherent rate vs. normal
resting HR
3. Atrial (Bainbridge reflex): Increased venous return to Atria causes stretch
reflex that signals SA node to make reflexive adjustments
As venous return increases, the pressure in the right atrium increases, which
stimulates the atrial stretch receptors .These receptors in turn signal the
medullary control centers to increase the heart rate

4. Baroreceptors(sense changes in blood pressure)and adjust autonomic system

for short term needs.
The baroreflex provides rapid reflex activity in the presence of blood pressure changes. When
elevated blood pressure is sensed, it causes the heart rate to decrease and thereby causes blood
pressure to decrease. A decrease in blood pressure decreases baroreflex activation and causes
heart rate to increase and to restore blood pressure levels.

Blood Vessel Overview

A. Blood vessel walls - three layers (tunics) that surround the lumen (central space)
1. tunica (intima) interna - innermost layer of vessel surrounding lumen;
This is continuous with the endocardial lining of the heart, and its flat cells
fit closely together, forming a slick surface to minimize friction of blood flow.
2. tunica media - concentric rings of smooth muscle and elastin; vasomotor
stimulation by sympathetic activation cause smooth muscle contraction and
vasoconstriction. Relaxation of smooth muscle causes vasodilation. This
layer greatly influences blood flow and blood pressure
3. tunica (adventitia) externa - composed chiefly of collagen with scattered
elastic bands. Helps to anchor vessels to surrounding structures and provides
for reinforcement and protection

B. Arteries - arteries and veins generally lie side by side to various regions of the
body; arteries differ from veins in that they have thicker walls (more smooth
muscle and elastin) that dont collapse when pinched. We see this during
cadaver inspection
1. Elastic (conducting) arteries - large arteries (up to 1 in. dia.) transporting large
volumes of blood (e.g. pulmonary and aortic trunks, common carotid, common
iliac arteries). Elastin is present in all three layers, but the tunica media contains
the most. This elastic property allows arteries to keep flow continuous as tubes
expand and recoil passively to accommodate changes in blood volume.

69

2. Muscular (distribution) arteries - medium-sized arteries (0.01 - 0.4 in. dia.) that
transport blood to skeletal muscle and internal organs (e.g. external carotid,
brachial, femoral, and mesenteric arteries). Proportionately, they have the thickest
tunica media so vasoconstriction is prominent and regulated by the sympathetic
nervous system.
3. Arterioles - small arteries with poorly defined tunica externa that vasoconstrict and
regulate the blood flow to the capillaries.

C. Capillaries - endothelial tubes enclosed in a delicate basement membrane

1. continuous capillaries - found in most regions of the body (e.g. skin and skeletal
muscle) with uninterrupted endothelial linings held together by tight junctions.
However, tight junctions are incomplete (except in blood-brain barrier)
so gaps (intercellular clefts) allow limited passage of fluids and small solutes.
2. fenestrated capillaries - endothelial cells are riddled with oval pores
(fenestrations) with a Swiss cheese appearance. These capillaries have much
greater permeability to fluids and proteins. Found in organs such as small
intestine, kidneys.
3. sinusoidal capillaries (sinusoids) - resemble fenestrated capillaries except they
also have irregular shaped lumens, fewer tight junctions, and large intercellular
clefts. Found in liver, bone marrow, spleen
70

4. capillary beds - each capillary is part of an interconnected network

A. Precapillary sphincters - constriction can reduce/stop blood flow, causing more
blood to flow through the preferred channel. ANS sympathetic control for emergency
or relaxation situations to perfuse or shunt blood depending on the organ needed.
B. True capillary vs metarteriole(vascular shunt):
1. Capillary: 10-100 per capillary bed and nutrient exchange occurs. Precapillary
sphincters open which allow blood to perfuse bed
2. Metarteriole: Precapillary sphincters constricted which routes blood through
channel directly bypassing capillary bed
3. Exercise vs Eating at level of stomach.

71

D. Veins
1. Venules - small postcapillary venules resemble expanded capillaries, lacking a
tunica media and externa. Common site for WBCs to congregate during
inflammation before they migrate into the inflamed area
2. Medium veins - thin tunica media with relatively few smooth muscle fibers. The
thickest layer is the tunica externa that contains elastic and collagen fibers. This
accounts for them being known as capacitance vessels or blood reservoirs.
3. Large veins - include the great veins (superior and inferior venae cavae, and their
tributaries within the abdominal and thoracic cavities); slender tunica media
surrounded by a thick tunica externa composed of elastin and collagen.
Low pressure adaptation: Due to large lumens and thin walls, maintenance of blood
pressure would be compromised if not for different adaptations (structural and functional)
Structural: A. Large lumens with thin walls offer little resistance to blood flow
B. Venous valves: One way valves that prevent backflow
Functional: A. Respiratory pump: Pressure changes in body cavities both squeeze
blood out, and at the same time allow more flow or input in an adjacent
cavity
B. Muscular pump: Contractions of skeletal muscle help propel the blood
through the system. The one way valves then prevent backflow
C. Smooth muscle around veins that respond to sympathetic control

72

Physiology of Circulation
Once the general outline of the circulatory system is mapped out, the properties that
regulate the blood flowing through the system, including the pressures needed to sustain
it, have several different physiologic and structural mechanisms.
1. Blood flow: Roughly the same as cardiac output when considering the system
wide application. Blood flow to specific organs can change however based on need.
2. Blood pressure: Force per unit area exerted on a vessel wall. Generally 120mm Hg
for systemic arterial pressure (during systole) Pressure is highest closest to heart
and decreases down its pressure gradient.
3. Resistance: The opposition of flow caused by friction in the systemic circuit.
A. Blood viscosity-- The thickness of the fluid. Increased thickening due to
pathologies would slow the rate of flow. The reverse is true when we look at
anemia (low blood cell count in some instances) and less resistance
B. Vessel Diameter-- Lumen size can affect resistance via normal or
pathological properties.
Normal: Blood flowing closest to lumen wall is slowed while blood in
center of lumen moves quicker. As noted earlier, the smaller arterioles
which respond to neural or chemical controls play a large role in
peripheral resistanc and therefore blood pressure
C. Length-- Longer the vessel the greater the resistance
Systemic Blood Pressure
Arterial BP: Reflects the rhythmic ejection of blood from left ventricle into the aorta and
has 2 factors.
1) The distensibility of the arteries closest to heart
2) The cardiac output (SVxHR)
Systolic BP defined as: How much pressure your blood is exerting against your artery
walls when the heart beats. Typical pressure= 120mm Hg
Diastolic BP defined as: How much pressure your blood is exerting against your artery
walls while the heart is resting between beats. Typical
pressure=80mm HG
Capillary BP: Decrease in pressure noted the further we move from heart. From
capillaries to capillary bed we see a drop from roughly 35-15mmHg. This drop is
required for 2 reasons
1) Fragile nature of capillary wall
2) Permeability of capillary wall requires little
pressure to move solutes

73

Pathophysiology 101
Hypertension: Primarily idiopathic in roughly 90% to 95% of cases. Classified as
>140/90 on 2 visits. Although the majority of cases have no specific etiology, several risk
factors have been shown to play a role:
High sodium intake
Obesity
Diabetes
Hypercholesterolemia
Smoking
Continuous stress
Personality traits
Pathogenesis: As noted in previous page, peripheral resistance plays a large role in
regulating blood pressure. Increased resistance due to narrowing of the arterioles is
the single most common characteristic of hypertension. As arterial BP is the product
of CO and peripheral resistance, hypertension involves hemodynamic mechanisms.
We may see an increase in cardiac output, peripheral resistance, or both
Constriction of arterioles.
1. SNS (sympathetic nervous system): Activation via psychogenic stress, or
autonomic response to baroreceptor(pressure sensors) changes.
a. Increased norepinephrine which constricts blood vessels
b. Epinephrine released by adrenal medulla resulting in increased heart
contraction/output
c. With prolonged hypertensive states, elastic tissue of arterioles has
been seen to be replaced by fibrinous collagen tissue.
c1. Thickened walls become less elastic which increases
blood pressure further as well as impeding tissue perfusion

2. Renin-angiotensin system: Thought to play a compensatory role via the

kidneys reaction to decreased tissue perfusion (blood flow) which they sense as
a drop in blood volume. Subsequently renin is secreted and angiotensin II is
formed. This leads to vasoconstriction in the renal system (further increasing
resistance). In addition it stimulates the release of aldosterone which results in
a further rise in blood pressure related to sodium and water retention.
Systolic Hypertension
SBP has been noted to rise between 30 and 84 years of age while diastolic BP levels off
post 50y/o. Age related changes affect not only BP measurements and their destructive
sxs but can also incur more serious cardiovascular events.
A) Rise in systolic due to loss of elastin in the vessel walls (much like in skin) which decreases
compliance to extensibility.
B) Decrease in systolic pressure means less stored energy for diastolic pressure
C) Increased systolic pressures require stronger contraction of ventricle. This accomplished by
possible hypertrophy which requires greater metabolic demand, and scenario where decreased
diastolic pressure limits coronary perfusion.

74

Orthostatic Hypotension
Abnormal drop in BP when moving from supine or seated position to standing and
impaired circulatory reflexes which decrease perfusion to brain. Symptoms would
include: Dizziness and/or syncope. Increased incidence in the elderly or those with
prolonged state of bedbound or wheelchair bound status.
Normal adaptive changes would include the
baroreceptors sensing the drop in BP as ~500 to
700ml of blood pools in trunk or LEs.
Causes:
1) Reduced blood volume: May be due to diuretics,
decreased thirst mechanism, loss of GI fluids due to
vomiting or diarrhea.
2) Pharmacologic agents: Anti-hypertensives,
antipyschotics, vasodilator drugs
3) Aging: Impaired cerebral blood flow (stenosis), inadequate fluid intake, large
carbohydrate rich meal(mechanism not fully understood yet)
4) Prolonged bed rest/immobility: Atrophy of LE musculature and decreased venous
pump, decreased resting venous tone
5) Autonomic disorders: Damage to the efferent sympathetic vasomotor fibers. SNS
normal response would be to increase HR/increase contractility/ and constrict some
regions of peripheral vasculature

Congestive Heart Failure: Condition in which the heart is unable to pump enough blood
to meet the bodies needs. Failure may occur on one or both sides of the heart. Not a
single disease but rather represents a group of pathologies or factors.
A. CAD (coronary atheroslcerosis): Fatty deposits that clog the coronary arteries
thereby impairing nutrient/oxygen delivery
B. Persistent HTN (hypertension): An increase in afterload (pressure on aortic and
pulmonary valves) causes the heart to have to work harder. Therefore hypertrophy of
the heart occurs for compensation due to increase in end systolic volume.
C. Multiple MI (myocardial infarction): Potential for MI's increases due to hypoxic
situation created by decreased O2 in coronary system.

75

Systolic Heart Failure-Cant pump

Impaired ejection of ventricle contents during systole due to decreased cardiac
contractility. The percentage or fraction of blood ejected would then be lower. Typical
amount is 60-65% of blood ejected under normal conditions. This is known as ejection
fraction.
Heart changes: Dilated ventricle due to
increased residual blood remaining in
ventricle. Subsequent increased wall
tension.
Diastolic Heart Failure-Cant fill
Impaired filling due to heart wall changes
cause higher incidence of congestion sxs.
More common in elderly persons, partly
because of increased collagen cross-linking
and loss of elastic fibers.
Heart changes: Small ventricular size and ventricular hypertrophy.
Abnormal hypertrophy demonstrates a haphazard organization of myofibrils which
impairs proper contractility
Right side heart failure vs Left side heart failure

76

11/9/2016

TheMuscularSystem

The function of muscles throughout the body perform several important tasks.
The anatomical makeup and distribution, or arrangement, are important not only
in their roles, but the actions about the joint/organ/structure they come into
contact with
Productionofmovement
Scanningstreetpriortoambulation
Adaptability:Graspingofnewborn
chickvsopeningstucklid
Bloodflowviamuscularcontraction
ofheart

Maintenanceofposture/position
Antigravitymusculature
Erectorspinae,soleus,abs
Standingonhillfacingupordown

Nearlycontinuousadjustment
MuscleTone

StabilizationofJoints
Includesmuscletone
Helpsequalizepressureduringjoint
movement

Generationofheat
Skeletalmusclemayaccountfor40%
ofbodymass
Byproductofmetabolismisheat
80%ofprocessisdegradedintoheat

Protectionoforgans
Abdominalcorset

11/9/2016

MuscleCellTypes
Skeletal:
Striated
Voluntary*
Roughly640

Cardiac:
Striated
Involuntary
Smooth:
Organ/Visceral
Nonstriated
Involuntary

SkeletalMuscleArrangement
Parallel: Fasciclesrunlongitudinally
Straplike:Nomusclebelly
Sartorius
Rectusabdominis
Zygomaticusmajor

Fusiform:Hasamusclebelly
Bicepbrachii
Gastrocnemius

Pennate: Fascicleattachobliquelytocentral
tendon(seenextslide)
Unipennate:Insertinto1sideoftendon
Bipennate:Insertsinto2sidesoftendon
Multipennate:Smalltendonsinsertintolargeone

Convergent: Broadoriginconvergesintoathin
tendon

11/9/2016

SkeletalMuscleBasicAnatomy
ExteriortoInteriorStructure
Connectivetissuesheathsaroundand
withineachintactmuscle
1. Epimysium
Denseconnectivetissuesurroundingeach
muscle
Mayblendwithdeeporsuperficialfascia
Mayfusedirectlytobone

2. Perimysium
Connectivetissuethatsurroundsbundlesof
musclefibers
KnownasaFascicle

3. Endomysium
Areolarconnectivetissuesurrounding
separateorindividual musclefibers

11/9/2016

SkeletalMuscleAttachment
DirectAttachment
Thefleshyepimysiumis
fuseddirectlytothe
periosteumofbone.
Ie:Subclavius,originofBicep
femoris,temporalis

IndirectAttachment
Connectivetissuewrappings
extendbeyondmuscle
Mostcommon
Functionalfor:
Smallsize
Toughcollagenfibersand
frictionresistance
Allowanceforother
tendons.Preservationof
jointspace

MuscleFiberAnatomy

11/9/2016

IndividualMuscleFiber
ExteriortoInteriorStructure
1. Sarcolema:Theplasma
membraneofthecell
Basementmembrane:Importantfor
mechanicalsupportandscaffolding
fortissuehealing
Sarcoplasmcontainsstored
glycogen/myoglobin/mitochondria
EntrypointsforTTubules

2. TTubules
ExtensionofSarcolema
Function:Topropagateaction
potentialsaroundandwithinmuscle
cell
APSpeedvsSpread
Lackofmyelinsheath
Depthand/orthicknessofmusclecell

IndividualMuscleFiber
ExteriortoInteriorStructure
3.SarcoplasmicReticulum(SR):A
membranousstructuresimilartoT
tubulesthatrunslongitudinally
StoragesiteforCa2+
CalciumPump: RemoveCa+
fromICFofmusclecellto(SR)
UseofCalsequestrin:High
capacityCa2+bindingprotein.
IsNot connectedtoextracellular
space
LateralendsareTerminalCisternae:
ExtrastorageforCa2+

Triad:Regioncomprising1Ttubuleand
2TerminalCisternae.Pointatwhichthe
APenteringcellcausesreleaseofCa2+
inhugeamountsfromSR

11/9/2016

TheMyofibril: Numerousmyofibrilsarewithin
eachmusclecell.Givemusclestheir
characteristicstriatedappearance duetolayout
ofsarcomeres (thesmallest contractileportion
ofmuscle)
ContractileProteinsormyofilaments
Myosin/ThickFilament

Sarcomere
HZone:MiddleofSarcomere.Centerpointis
Mline.Linkscentralportionofthickfilaments
together
ABand:RegionofoverlappingThick(myosin)
andThin(actin)filaments
IBand:RegiononeithersideofZdisc.Thin
filamentsandsupportproteinsonly

Actin/ThinFilament

Portionthatshortenswithcontraction

ZDisc(line):Markstheendofeach
sarcomere

ContractileProteins
ThickFilaments:Myosin
Largemolecularweight
proteinwithatotalof6
polypeptidechains
Themolecularmotor for
movement
A.Pairofheavychainsform
tail
B.Lightchains(2pair)
Globularheadwithbindingsites
Actinsite
ATPsite

11/9/2016

ContractileProteins
ThinFilaments:Actin
Comprisedof3proteins.
similarhelicalshapeasmyosin
A.Actin:Globularproteinwith
myosinbindingsites
Function:Bindingforcross
bridgeformation

B.Tropomyosin:Filament
proteinthattwistsalongactin
toblockbindingsite
C.Troponin:3Different
proteinsthatassistin
regulatingmyosinattachment
(seenextslide)

ContractileProteins:TroponinComplex
A.TroponinT: Attaches

troponincomplextotropomyosin
B.TroponinI:Inhibitoryprotein
thatcoversbindingsite
C.TroponinC:Calcium binding
protein
Action:
1.Influxofcalciumbindsto
TroponinC
2.Conformationalchangeto
structure
3.RotatesTropomyosinaway
frombindingsiteswhichallows
myosinheadtoattach

11/9/2016

ContractileProteinArrangement

AccessoryProteins
Actinin:Anchorsthin
filamenttoZdisk
Nebulin:Liesalongsideof
actintomaintainalignment
Titin:Anchorsthickfilament
toZdisc.Iselasticwhich
assistinreturning
sarcomeretorestinglength
postactivity
Dystrophin:Linkfilament
Anchorsactintocell
membrane
Transmitsmusclecontraction
forcetocellmembraneand
extracellularmatrix

11/9/2016

MuscleFiberActivation

Fromthoughttoaction:The
neuromuscularjunction
1. NerveStimulus:Actionpotential(AP)

PropagationofAPalongmyelinatedmotor
neuron

2. ActionofvoltagegatedCa2+channels

InfluxofCa2+

3. Calciuminfluxcausesneurotransmitter
vesiclestobindtomembrane

Exocytosisreleases(acetylcholine)into
cleft

4&5.ACHbindstoligandchannelon
postsynapticmembranewhich
unlocksgateforNa+influx
6. Localdepolarization/endplatepotential
7. VoltagealongmembraneopensNa+
channelwhichproducesAP

11/9/2016

ExcitationContractionCoupling
1. Spreadoflocalcurrentalongmusclecell
sarcolemaextendsintoandaroundthe
muscleviaTtubules
2. Voltagesensitiveproteinsintubule
changeshapewhichfacilitatesthe
openingofcalciumchannelsinterminal
cisternaeandsarcoplasmicreticulum
3. CalciumentertheICFofmusclefiberand
contactsTroponinC
4. TroponinCundergoesitsown
conformationchangeandrotates
tropomyosinawayfrommyosinbinding
sites
5. Myosin(thickfilament)headcanthen
attach

CrossBridgeCycle/SlidingFilament
1. ATPbindstomyosinheadreleasingitfrom
actin
2. HydrolysisofATPtoADP&Picauseshead
toreturntocockedposition
3. Thenowenergizedheadattachesto
exposedsiteonactin

4.
5.
6.

Multiplecrossbridgesareformed
ADPandPiarereleasedwhichgivethe
powerstrokeofroughly45degtopull
actinclosertoMline
Processrepeatsitself

Videolink:
https://www.youtube.com/watch?v=gJ309LfHQ
3M

10

11/9/2016

TheMotorUnit
Definedasthemotorneuronandallthe
musclefibersitinnervates.Theamount
offiberssuppliedbyasinglemotor
neuronisdependentonthedegreeof
controlandstrengthnecessaryfortask.
IE:TheeyeMinimalamountoffibers
Theglutesmodtomaxamountof
fibers
SizePrinciple/Recruitment:Themore
motorunitsrecruited,thegreater
degreeofforceortensionavailable

StimulusFrequency

StimulusStrength

Ingeneral,voluntarychangesinstrengthor
speedofcontractioncanbealteredbytwo
processes
.Twitch:SingleAP=Singlebrieffibertwitch
A. Temporal(wave)summation:Frequencyof
APincreaseswithsubsequentincreasein
Ca2+
B. Buildingofmusclecontraction:Muscle
twitchof2nd APridesontopof1st.
C. TimedifferencebetweenspeedofAPand
muscletwitchallowsforsmooth
movement

A. Recruitmentbasedonsizeoftask:
LiftingboxofStyrofoamvsboxofbooks
B. Smaller/moreexcitablefibersrecruited
first
C. Larger/leastexcitable(highest
threshold)recruitedasneeded
D. Posturalimportance:Smallermuscle
fibersrequirelessenergy.Multiple
smallposturaladjustmentsbetter
servedbysmallermusclegroups

11

11/16/2016

ConcentricvsEccentricWork

11/16/2016

EccentricContractionTheory
Initialknowncrossbridgecycle
formation
Natureoftask/activitycallsfor
controlledlengtheningofmuscle
Theory
Boundmyosinnotallowedtodetach
duetoforceofelongation
Subsequentdetachmentwithoutloss
ofADP+Pi
Reattachmenttonextbindingsite.
Processrepeats
EventuallossofADP+Pi andanother
ATPstartsprocessagain

Supportiveresearch:
Lessmuscleactivityrequiredto
maintainforce
Fewerfibersrecruited

Musclefibertypes:RedMuscle

Musclefibertypes:WhiteMuscle

Function:

Function:

Endurance
Posture

Characteristics
Redfibers
Richcapillarynetwork
Myoglobin:Oxygenbindingprotein

Shorttermuseforintense/powerful
movements
Quicklyfatigue

Characteristics
Whitefibers
Decreasedcapillarynetwork

Contractionspeed:Slowtofast

Contractionspeed:Fast

PrimarypathwayforATPproduction

PrimarypathwayforATPproduction

Aerobic*/Citricacidcycle

Anaerobicglycolysis

11/16/2016

FuelSupplyforMuscles
Theprimarysourceoffuelfor
muscleactivityisATP(adenosine
triphosphate)
1. Requiredforcontractile
activity
2. Servesasfuelforcalcium
pumpsinsarcoplasmic
reticulum
Fuelsupplymaintainedbysystems
adaptedtophysicaldemands
Enduranceactivity=Longterm
supply

Vs.

Prius

Brief/vigorousactivity=
Frequentfuelreplenishment
Ferrari

11/16/2016

DirectPhosphorylationofADP:ImmediateNeed
RestingATPreserverelatively
low.(thinkhomeostasis)
Fuelforroughly46seconds
Demandmayquicklyoutstrip
supply.
Processrequiredtogenerate
ATPataspeedequaltotask
1. ADPasremnantofrecent
crossbridgecycle
2. Poolofcreatine phosphate
(CP)
3. Transferofphosphateenergy
andcreationofoneATP

AnaerobicGlycolysis:Shortdurationactivity
Demandhasnowoutpacedthe
ADPandCPpathwayandan
optionisrequiredforafuel
systemthatdoesnotrequire
oxygen
Foodforfuel:Glucose=sugar
Fuelforroughly3040seconds
Processrequiredtogenerate
ATPataspeedequaltotask
1. Glycogenorglucosebroken
downforming2ATP
2. Pyruvicacidremains
howeverunabletoreenter
mitochondriaforproduction
ofmoreATP
3. Lacticacidisbyproductof
convertedpyruvicacid

11/16/2016

AerobicRespiration:Extendeddurationactivity
Prolongedactivityrequires
steadyflowofenergy.Oxygen
isunderstandablyrequiredfor
thisprocess
Foodforfuel:Glucose,
pyruvicacid,aminoacids,
fattyacids
Fuelforhours
1. Occursinmitochondria
2. Productionof32ATP*
3. Lowlevelactivityallows
bloodsupplytobring
nutrientstomuscles

MuscleSystemChanges&ImpairedFunction

11/16/2016

Theeffectsofagingonskeletalmuscle
Projectedchangesinelderlypopulation
by2050
2billionpeople>60yearsold
400million>80yearold
Withagecomesanincreaseinnormal
andabnormalmusculoskeletalchanges
andchallenges
ADLdeficits
Disabilities

FunctionalChanges
1. Decreaseinmuscleandbonemass
2. Relativeincreaseinbodyfat
3. Generalmuscleweakness=2.5
greaterriskofseveremobility
impairment
4timesgreaterriskofdecreasedgait
velocity
2timesgreaterriskofmortality

Theeffectsofagingonskeletalmuscle
Severalfactorsmustbeconsidered
howeverapartfromgeneralatrophyof
muscles
Peripheralnerveimpairment
RememberPVD

Changesinneuromuscularjunction
ResponsibleforAPs

Fatinfiltration
Effectoncontractility

Cellularchanges
Musclefiberchange

Sarcopenia:Lossofleanbodymass
withaging
*Notuniversal

11/16/2016

SatelliteCells:Importantformusclecell
homeostasisandregeneration.
Normallyinrestingstatehowever
activatedunderstress
Possibilityfordecreasednumbertherefore
impairedregeneration/repair

Reductionseenmoreofteninfast
twitch musclefibers
Impactonfunction
Impactonfallrisk

11/16/2016

Musclefiberatrophyandpowerloss
Musclemasslossmostprominentin
lowerlimbs.Upwardsof3040%loss
offibernumber by8th decadeoflife
Mitochondrialcelldeath
Decreaseinnutrientpathwayfor
muscleenergy

DecreaseinTypeII(fasttwitch)
musclefibers
Musclefibertransformation
Changesinresponsetoexternal
stimuli
TypeIaffectedbyinactivity
TypeIIaffectedbyaging,disease

PredominanceforTypeIIatrophy

Musclefiberaginganddysfunction
Fatinfiltration
Increaseinbothintermuscularand
intramuscularfatdeposition
Reducedmuscleforcehowever
researchongoingonwhy

Noncontractiletissueinfiltration
Connectivetissue
Decreasedforceproduction
Increasedimmobilityormuscle
lengthimbalance
Fallrisk?

11/16/2016

MotorSystemAbnormalities:MuscularDystrophy

MuscularDystrophy
Largestandmostcommonclassof
progressiveneuromusculardisordersof
childhoodthatareinherited.Characterized
bymuscleweakness/wasting
Types:DuchenneandBecker mostcommon
Characteristics
Asnotedtoright
Relativelysymmetricmusclewasting
Proximalmusclesmoreaffectedwith
Beckerhowevermilderform
Exclusivetomales.Veryrareinfemales
DisorderofDystrophinandSarcolema

11/16/2016

MuscularDystrophyandFiber
Geneticdefectwithcytoskeletallink
proteindystrophin.
Dystrophinlinksactintosarcolemaand
assistinkeepingalignmentofcell
componentsduringmovement
Duchenne:Absentdystrophin
Becker:Abnormalityofdystrophin
Musclemovementcausescascadeof
effects
a. Damagetosarcolema

Mechanicalcauseoftissuedeath

b. Destabilizationofmembrane

AlterationinCa2+levels

c. Fatandconnectivetissuecells
accumulatebetweendamaged
musclefibers

MuscularDystrophyPresentation
1. Weaknessandlowtone
2. Gowerssign(walkingupLEs)
3. Trendelenburggait
4. Scoliosis
5. Pseudohypertrophy
6. Contractures:Inorderoffrequency

Ankleplantarflexion
Kneeflexion
Hipflexion
Elbowandwristflexion

10

Nov23,2016
AHCJ375

Name:__________________
StudentID:______________

Physiology
Quiz5

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

TypeIslowtwitchmusclefibersarecharacterizedbyallexcept
A.Anaerobicglycolysisforfuel

B.Aerobicrespirationforfuel
C.Fatigueresistant

D.Richcapillarynetwork
Thedecreaseinsatellitecellsseeninelderlyskeletalmusclehasthebiggestimpact
on(a.reductioninslowtwitchfiber/b.reductioninfasttwitchfibers)
T/FPosturalorantigravitymusclesrelymainlyonwhitemusclefibersforfunction

Thefuelsystemthatprovidesenergyforactivityspanning3040secondsis
A.Creatinephosphate/Directphosphorylation

B.Aerobicrespiration
C.Anaerobicglycolysis
Pseduohypertrophy(ie:enlargedcalfsize)duetofatdepositioniscommonlyassociated
with
A.Contracturesandfattydepositswithinmuscle B.Cerebralpalsy

C.Deconditioningandlossofmuscletofatratio D.Musculardystrophy

Thelossofmusclepowerandgreaterspecificmusclefiberatrophyintheelderlyisseen
primarilyin
A.Fasttwitch

B.Slowtwitch
Apatientwithmusculardystrophywouldmostlikelyfitwhatcharacteristic
A.Distalmusclewasting

B.Unilateralmusclewasting
C.Havingincreasedmuscletoneduetospasticity D.Symmetricmusclewasting
Inmusculardystrophy,thepatientthatrequiresincreaseduseofhisarmstocometoa
standfromthefloorwouldbepositiveforwhatclinicalsign
A.Lowtone B.GowerssignC.Trendelenburggait
D.Pseduohypertrophy
Musculardystrophyaffectswhatcomponentofmuscletissue
A.Terminalcisternae B.Actin
C.Myosin
D.Dystrophin

Redmusclefiberswouldbenefitfromallthefollowingexcept
A.Useofglucose/aminoacids/fattyacidsforfuel B.Abundanceofmitochondria
C.Decreasedcapillarynetwork
D.Increasedmyoglobincontent

Nov15,2016
AHCJ375

Name:__________________
StudentID:______________

Physiology:Quiz5

1.

2.

3.

4.

5.

6.

7.

8.

9.

10.

T/FTheepimysiumistheconnectivetissuethatsurroundsthemusclethatblendsinto

deepfasciaorbone
WhichoftheseisNOTapartoftheactinmyofilament?
A.actin
B.terminalcisternae
C.tropomyosinD.troponin
Inskeletalmuscle,calciumionarestoredin(A.Ttubules/B.Sarcoplasmicreticulum)
Forcrossbridgerelease,itisnecessaryfor__________toattachtothemyosinhead.
A.atropomyosinmolecule B.Ca2+ions C.atroponinmoleculeD.ATP
Thestructurethatmarkstheendofthesarcomereis
A.MLine

B.ABand
C.Zdisc

D.IBand

Thespreadoflocalcurrentfromtheexteriorofthemusclecelltotheinteriorisdoneby
A.Sarcoplasmicreticulum B.TerminalCisternae
C.Sarcolema

D.Ttubules
T/FThemovementoftropomyosinawayfromthemyosinbindingsitesisdonebythe

attachmentofsodiumions
Whichoftheseregionsshorten(s)duringskeletalmusclecontraction?
A.Aband
B.Hzone
C.Iband
D.Mline

Themostcommonformofmuscleattachmentis(A.Indirect/B.Direct)

Theneurotransmitteracetylcholine(ACH)isreleasedfromtheaxonterminalatthe
neuromuscularjunctionby(A.Calciumioninflux/B.Sodiumioninflux)

E.C.Giventheseevents:
1.Actionpotentialtravelsalongthesarcolema
2.Ttubulesundergodepolarization
3.voltagegatedCa2+ionchannelsinsarcoplasmicreticulumopen
4.Ca2+ionsdiffuseintothesarcoplasm
5.Ca2+ionsbindtotroponinmolecules

Choosethearrangementthatliststheseeventsintheordertheyoccurfollowingasinglestimulationof
askeletalmusclecell.

A)

1,2,3,4,5

B)

1,3,5,4,2

D)

3,1,5,2,4

E)

4,5,12,3

C)

2,1,3,4,5


E.C.Giventheseevents:
1.activesitesonactinmyofilamentareexposed
2.actinmyofilamentslidesovermyosinmyofilament
3.Ca2+ionbindstotroponin
4.myosinheadsmove
5.crossbridgesform

Choosethearrangementthatliststhecorrectorderinwhichtheyoccurduringasinglestimulationofa
skeletalmuscle.

A)
4,3,2,1,5
B)
3,1,5,4,2
C)
3,2,5,4,1

D)

2,4,3,5,1

E)

1,2,3,4,5

E.C.WhichofthefollowingbestdescribestheroleofCa2+inmusclecontraction?

A)

Itbindstotropomyosin,movingtroponin,sothatmyosinheadscanbindtoactin.

B)

Itbindstotropomyosin,movingtroponin,sothatactinheadscanbindtomyosin.

C)

Itbindstotroponin,movingtropomyosin,sothatmyosinheadscanbindtoactin.

D)

Itbindstotroponin,movingtropomyosin,sothatactinheadscanbindtomyosin.

E)

Itbindstoactin,movingmyosin,sothattroponincanbindtotropomyosin.