Test 3 Lecture Flashcards
serves as the pump that imparts pressure to move the blood to the tissues
Heart
the conveyance through which blood travels
Blood vessels
carry blood away from the heart
Arteries
return blood to the heart
Veins
medium to transport materials long distance in the body
Blood
prevents blood from mixing from the two sides
septum
Located centrally in the thoracic cavity
Heart
Left s rich in
oxygenated blood
Right is
deoxygenated
receive blood returning to the heart
Atria (upper chamber)
carry blood to atria
veins
pump blood from the heart
ventricles (lower chamber)
carry blood from ventricles
arteries
heart to lung
pulmonary circulation
herat to body
systemic circulation
systemic circulation pathway
Aorta Branching arteries Systemic capillaries (gas exchange: O2-rich to O2-poor blood) Systemic veins Vena Cavae
vein carries blood from the digestive tract to the liver so absorbed nutrients can be processed
Hepatic portal
difference in pressure between the beginning and end of the vessel
Pressure gradient (Delta P)
Blood flows from an area of high pressure to an area of low pressure
Pressure gradient
Heart is responsible for creating the high pressure
True
Equally exerted in all directions
hydrostatic pressure c
A moving fluid has two components
A flowing component representing its kinetic energy
And a lateral component that represents its hydrostatic pressure (& potential energy)
Pressure changes without changing volume
True
Contracting the wall of a fluid-filled container increases the pressure on the fluid without changing its volume
True
Expanding the wall of a fluid-filled container decreases the pressure on the fluid
True
gradient is the difference in pressure between two ends of a tube
pressure gradient
The higher the pressure gradient the greater the flow
direct relationship
The hindrance or opposition to blood flow due to friction between the fluid & vessel walls
Resistance R
Inverse relationship between flow and resistance
RR
3 factors determine resistance
Vessel radius
Vessel length
viscocity
decrease in the radius; increases resistance
Vasoconstriction
increase in radius; decreases resistance
vasodilation
Blood flow is directly proportional to the pressure gradient and indirectly proportional to the resistance of the vessel
Blood flow
the volume of blood passing a given point per unit time.
How much
Expressed as volume/unit time (L/min)
Flow
the distance a fixed volume of blood travels in a given unit of time
Velocity of flow
is a muscular organ about the size of a fist located in the center of the thoracic cavity
Heart
a double walled sac enclosing the heart
Pericardium
Pericardium functions
Protect the heart
Anchor it to the surrounding structures
Prevents overfilling
Between the two layers is the pericardial cavity filled with serous fluid
composed of cardiac muscle bundles & a fibrous connective tissue network that forms a fibrous skeleton for the heart muscle
Myocardium
Spirally arranged around the circumference of the heart
Contraction, results in a wringing effect that pushes blood upward to the arteries
myocardium
are the receiving chambers for blood returning from the circulation
atria (superior)
receives blood from the systemic circulation (deoxygenated)
right atria
receives blood from the pulmonary circulation (oxygenated)
left atria
The contractions of the atria contribute very little to the propulsion of blood by the heart
true
are the propelling chambers for the blood returning to circulation
Ventricles
ventricle pumps blood to the pulmonary circulation (deoxygenated)
Right ventricle
ventricle pumps blood to the
left ventricle
Aided by one-way valves
Greater pressure behind the valve causes the valve to open
Greater pressure in front of the valve causes the valve to close
blood flow is unidirectional
Located between the atrium and ventricles
atrioventricular valves
is also called mitral valve
left
also called tricuspid valve
right
Lie at the junction between the arteries & the ventricles
semlunar valves
Leaving left ventricle is called
aortic valve
Leaving right ventricle is called
pulmonary valve
Back-flow creates pressure on the cusps that hold them shut
true
There are no valves between veins and atria
true
Atrial pressure not much higher than venous pressure
true
becomes partially compressed during atrial contraction
vaena caeva
Atrial muscle anchored
above the rings
Ventricular muscle anchored
below the rings
Uninucleate and smaller than skeletal muscle
cardiac muscle
mechanical junctions to hold the cells together
desmosomes
allow AP to spread between cells
gap junction
are larger than those found in skeletal muscle
T-tubules
the volume of a cardiac muscle cell are mitochondria
1/3
99% muscle cells
Do mechanical work of pumping
Do not initiate their own AP
contractile cells
Specialized cells that initiate & conduct APs
Display pacemaker activity
autorhythmic cells
Voltage-gated Na+ channels open to allow Na+ influx (permeability rapidly plummets after an action)
Rapid rising phase
positive level is maintained close to initial peak by the slow L-type Ca2+ channels & decreased K+ permeability
Results in a plateau
Plateau phase
inactivation of Ca2+ channels & delayed activation of K+ channels
Rapid falling phase
During refractory period, a 2nd AP can not be triggered until an excitable membrane has recovered
true
3 ions
Na+, K+, Ca2+
allows for the movement of cations. In the pacemaker cell, allows a constant, passive influx of Na+ into the cell throughout the cycle
If channels (Na+ leak channels)
slow opening channels that allow an efflux of K+ out of the cell; results in a repolarization
K+ channels (voltage-gated)
+ channels (voltage-gated) – open prior to threshold causing membrane to reach threshold
T-type Ca
channels (voltage-gated) – open causing the rapid rising phase of the action potential
L–typed Ca
Sympathetic stimulation
Increased Na+ and Ca2+ permeability in the pacemaker cells
Decreased K+ permeability resulting in depolarizing effect
Increases conductive velocity at the AV node (and beyond) to ventricles (using the above mechanics)
Increases Ca2+ permeability thereby increasing contractile strength
heart beats faster
end result
parasympathetic stumulation
Decreased Na+ and Ca2+ permeability in the pacemaker cells
Enhanced K+ permeability resulting in hyperpolarization
Prolongs transmission of excitation from AV node to ventricles (using the above mechanics)
Reduces the slow inward current of Ca2+ (shrinks the plateau phase of the AP)
End result
heart beat less rapidly
specialized region in the right atrial wall near the opening at the superior venae cavae
SA node (Sinoatrial node)
located at the base of the right atrium near the septum; above the junction of the atrium & ventricles
AV node
– tract of cells that originate at the AV node. Divides into two branches down to the tip of the ventricle and back towards the atria
Bundle of His (atrioventricular bundle)
terminal fibers that extend from the Bundle of His
Purkinje fibers
pacemaker
SA node
features of SA node
Sets the rate for the rest of the heart
Other nodes have their own natural slower rates, but rate is directed by SA node
If the SA node is damaged, the next fastest node sets the pace.
Once initiated in the SA node, an AP spreads throughout the rest of the heart
Contractile efficiency satisfies 3 criteria
Atrial excitation & contraction should be complete before the onset of ventricular contraction
Excitation of cardiac muscle fibers should be coordinated to ensure that each heart chamber contracts as a unit to pump efficiently
The pair of atria & pair of ventricles should be functionally coordinated so that both members of the pair contract simultaneously
AP originating in the SA node first spreads throughout both atria via
gap junctions (cell to cell)
Two conduction pathways speed up conduction
Interatrial pathway
Internodal pathway
SA node to left atrium
Rapidly transmits AP so that both atria depolarize to contract simultaneously
Interatrial pathway
SA node to AV node
Only point of electrical contact between atria and ventricles
Ensures sequential contracting of the ventricles following atrial contraction
Internodal pathway
Causes a delay which enables atria to completely depolarize & contract before ventricles do
AV nodal delay
At the AV node, the AP is conducted relatively slowly
Causes a delay (called the AV nodal delay) which enables atria to completely depolarize & contract before ventricles do
Impulse travels rapidly down Bundles of His & purkinje fibers to the ventricular myocardium
Ensures that the ventricles contract as a unit
Does not travel to all cells – done by gap junctions from excited cells
More highly organized
Ventricular mass > atrial mass
Ensures a single, smooth, coordinated contraction that simultaneously ejects blood into the pulmonary & system circulation
Ventricular excitation
Recording of the electrical currents generated by cardiac muscles
The Electrocardiogram (ECG)
A recording of the electrical activity induced in the body fluids by the cardiac muscles that reaches the surface… NOT a direct recording of electrical activity of the heart
An overall spread of activity throughout the heart during depolarization and hyperpolarization… NOT a recording of a single AP
Comparison in voltage detected by electrodes at two different points
ECG
3 distinct wave forms
P wave: atrial depolarization
QRS complex: ventricular depolarization
T wave: ventricular repolarization
important notes to think about
Firing of the SA node is not detectable
No separate wave for atrial repolarization (masked by QRS complex)
P wave is smaller than QRS because atria have less mass & generate less electrical activity
PR segment: AV nodal delay
ST segment: plateau phase of ventricular contractile cells
TP interval: heart is at rest & ventricular filling is taking place
No net current flow during 3 periods
counting the number of peaks of a specific wave form over a period of a minute (e.g. P wave or R peak in QRS complex). Is it between 60-100 beats/min, resting.
heart rate
– any interruptions in spacing of the P→QRS→T waves
irregular rhythm
Looking for the presence of the individual waves
ECG
Is each P wave followed by a QRS complex. Lack of QRS suggests
a transmission problem in the AV node
can be determined by the distance between QRS complexes
Abnormalities of rates
rapid heart rate
tachycardia
slowed heart rate
bradycardia
variations from the norm in regards to ECG waves
abnormalities in rhythm
– no definitive P waves resulting from irregular uncoordinated depolarization
a fib
no detectable pattern or rhythm resulting from irregular uncoordinated chaotic contractions
Ventricular fibrillation
atria contract faster than ventricles and thus not all impulses are translated by to the ventricles (due to refractory period)
atria flutters
ventricles fail to be stimulated & thus fail to contract
heart blocks
damage to the heart muscle
cardiac myopathy
Abnormal QRS waveforms because the muscle is unable to contract properly as a result of damaged or necrotic tissue
cardiac myopathy
contraction and emptying; spread of excitation
systole
relaxation and filling; subsequent repolarization
diastole
Usually referring to ventricles unless otherwise stated
Both atria and ventricles have their own cycles of systole and diastole
TP interval
Atrial pressure > ventricular pressure (due to venous inflow)
AV valve is open
Ventricular volume increases
Mid-ventricular diastole
Corresponds to the P wave
Atrial contraction
Atrial pressure increases and more blood is pushed into the ventricle
Rise in ventricular pressure
Atrial pressure > ventricular pressure (due to venous inflow)
AV valve is open
Late ventricular diastole
Volume of blood in the ventricle at the end of diastole
End-Diastolic Volume (EDV)
Corresponds to the QRS complex Beginning of ventricular systole Impulse travels to AV node & beyond to excite the ventricle Sharp increase in ventricular pressure Closing of the AV valve
Ventricular excitation
Ventricular pressure must be greater than aortic pressure to open aortic valve
No blood enters or leaves
Muscles don’t change length
Isometric ventricular contraction
Ventricular pressure > aortic pressure
Aortic valve opens
Ventricular volume decreases
Subsequent rise in aortic pressure (resulting from the blood volume increasing faster than it is leaving the aorta)
Blood volume ejected is called the stroke volume
ventricular ejection
Not all of the blood is ejected during the systole
End of ventricular systole
Volume of blood in the ventricle at the end of systole
ESV
(stroke volume) or the amount of blood pumped per contraction
EDV – ESV = SV
Corresponds to the T wave
Ventricular repolarization
Results in slight disturbance in aortic pressure curve
docrotic notch
Corresponds to the T wave
Onset of diastole
Ventricular pressure
Ventricular repolarization
Both the AV and aortic valves are closed
No blood enters or leaves
Isovolumetric ventricular relaxation
Ventricular pressure
Ventricular filling
Most ventricular filling occurs early
daistole
If heart rate increases, diastole time decreases
BUT this doesn’t affect the fill volume
The amount of blood pumped per minute
cardiac output
cardiac output formula
CO = HR x SV
cardiac output is
Dependent on heart rate and stroke volume
Heart rate is determined by _____influence on the SA node
autonomic
primarily supplies atrium (esp. SA & AV nodes) as well as the ventricles (sparsely innervated)
Parasympathetic innervation (via Vagus nerve)
supplies the atria and ventricles
Sympathetic innervation
inhibits heart rate
parasympathetic fibers
increases heart rate
sympathetic fibers
Control of heart rate
Antagonistic autonomic control
Determined by the extent of venous return and sympathetic activity
stroke volume
inherent ability of the heart to control stroke volume
intrinsic
the heart pumps out the volume of blood during systole, the amount that is returned to it during diastole
Increase venous return (stretch) → increase stroke volume (force)
Frank Starling Law
results from sympathetic stimulation
Extrinsic
Enhancing contraction strength thus ejecting a greater volume (and enhancing venous return)
Extrinsic
Sympathetically-induced venous vasoconstriction
Modest elevation of venous pressure → increased DP to drive more blood to heart → increased venous return
Decreased venous capacity → increased blood flow → increased venous return
Increased cardiac output → helps sustain increased venous return
Muscle contraction yields external venous compression
AKA skeletal muscle pump
Pushes blood out of veins to heart
Skeletal muscle activity
Pressure within the chest is 5 mm Hg less than ATM
Creates a pressure gradient towards the chest that promotes venous return
Respiratory activity
blood from heart to organs
arteries
smaller arteries of the organs receiving blood supply
arterioles
smaller vessels; exchanges between blood and organs
capilliaries
carry blood from the organs
venules
convergence of venules to return blood to heart
veins
Composed of layers of smooth muscle, epithelium and connective tissues
blood vessels
Inner most layer of all blood vessels is epithelium called
endothelium
which plays an important role in regulating blood pressure through paracrines
endothelium
surrounds the epithelium in most vessels which modulate the diameter of the vessel
smooth muscle
allows vessels to stretch and recoil
elastic connective tissue
resists stretch
fibrous connective
arteries 2 function
Rapid transit for blood from heart to organs Pressure reservoir (due to elasticity of the vessel) to drive blood forward when heart is relaxing
are the major resistance organs due to their small radii
arterioles
Responsible for converting the pulsatile pressure in arteries into a nonfluctuating pressure in capillaries
Marked drop in mean pressure encourages blood flow from heart to organs
arterioles
Radii (& thus resistance) can be adjusted independently to
Variably distribute cardiac output among systemic organs dependent on need
Help to regulate arteriole pressure
are small arteriole-like vessels possessing very little smooth muscle that form precapillary sphincters
metaarterioles
regulate blood flow into the capillary beds in response to metabolic change
precapilliary sphincters
narrowing of the vessel
vasoconstriction
enlargement of vessel
vasodilation
baseline arteriole resistance
vascular tone (partial constriction)
vascular tone depends on 2 factors
self induced activity and sympathetic fibers
Primary site for material exchange (primarily by diffusion)
capilliaries
no cell is further than ~10 μm from a capillary
extensive branching
Increased surface area for exchange due to the massive networks
Slow blood flow (velocity of flow mm/sec) NOT flow rate (liters/min)
capiliaries function
Capillaries drain into venules
Have little tone & resistance
Extensive communication between arterioles & venules via chemical signals to match inflow ; outflow
venules
Large in radius
Little resistance to flow
Serves as a blood reservoir
Veins
Allow blood to move towards the heart & prevent backward flow despite the low pressure in veins
Venous valves
venous valves
One-way valves
2-4 cm apart
Counteracts gravitational effects
provides tensile strength against the high pressure caused by blood leaving from the heart
collagen
provides elasticity
elastin
When blood leaves heart during systole, more blood enters arteries than is leaving (due to R in smaller vessels) therefore
arteries expand temporarily
During heart relaxation, arteries passively recoil to ensure
continuous blood flow
pressure exerted in the arteries when blood is ejected into them during ventricular systole (maximum pressure)
systolic pressure
pressure within the arteries when blood is draining into the rest of the vessels during ventricular diastole (minimum pressure)
diastolic pressure
pressure difference between systolic and diastolic pressure
pulse pressure
average pressure driving blood forward
MAP Mean Arterial pressure
sounds are used to determine the blood pressure
korotkoff
pressure is the blood pressure monitored & regulated in the body
mean arterial pressure
determined by heart rate & stroke volume
cardiac output
resistance determined by the diameter of the arterioles
Peripheral resistance
↑ blood volume yields
↑ blood pressure
Blood distribution is determined by
diameter of vein
Matches tissue blood flow to metabolic needs
Accomplished through paracrines and myogenic autoregulation
local control
Neural control maintaining mean arterial pressure & blood distribution
sympathetic reflexes
Regulating resistance through catecholamines & other hormones
Regulation of solute and water balance by the kidneys to influence blood pressure
hormones
increased blood flow resulting from increased metabolic need
active hypermia
increase in blood flow after an occlusion
reactive hyperemia
local arteriolar mechanisms that keep tissue blood flow fairly constant despite variations in mean arterial driving pressure
myogenic autoregulation
The local chemical changes are detected and release paracrine factors that influence nearby smooth muscle
endothelial cells
Causes arteriolar vasodilation by inhibiting Ca2+ movement into the smooth muscle
NO
Causes arteriolar vasoconstriction
Endothilin
NorE on smooth muscles
Acts on a1 adrenergic receptors
Results in vasoconstriction
Only exception is brain that doesn’t have a1 receptors
Neural Reflex
release epinephrine & norepinephrine
adrenal medulla
generalized vasoconstriction
Localized in digestive organs & kidneys
The a1 receptors
reinforce local vasodilation
b2 receptors
results in increased arteriolar pressure
Increased H2O retention
Released from posterior pituitary
Potent vasoconstrictor
Primarily involved in regulating H2O balance promoting H2O retention
Vasopressin (anti-diuretic hormone, ADH)
Part of a larger solute/water regulatory system
Potent vasoconstrictor
Regulates salt balance promoting water retention
Angiotensin II
organs that provide nutrients and remove waste & heat
reconditioning organs
Learn Blood Flow
notes
joined together with leaky junction. Most common. In neural tissue, evolved tight junctions to form the blood brain barrier
Continuous capillaries
capillaries possess large pores to allow high volumes of fluid to pass between the plasma and IF. Located predominantly in kidney andintestine
Fenestrated capillaries
have large gaps between cells which allow blood cells, proteins, and plasma to cross
Sinusoids
Material exchange
Exchangeable proteins move through capillary endothelium by vesicular transport (transcytosis)
Lipid soluble substances pass through
Gases diffuse through the epithelium and via cell junctions
Capillary pores/junctions permit the passage of small H2O soluble substances to pass through
Two mechanisms for capillary exchange
Two mechanisms for capillary exchange
Bulk flow
Passive diffusion & vesicular transport
Down concentration gradients
Exchange of individual solutes
Movement of plasma out of capillaries (filtration) & interstitial fluid into the capillaries (absorption)
Plasma mixes with interstitial fluid
Dependent on pressure inside and outside of capillary
Important role in regulating the distribution of the ECF and thus helps to maintain arterial blood pressure
Bulk Flow
