Exam 1 Flashcards
What type of loop is the CVS
Closed loop
Functions of the CVS
Transport of materials
Communication between cells
What does the CVS transport
Nutrients (Macros)
Wastes (CO2)
Water
Gases (O2)
Heat (sweat, shivering)
How does CVS contribute to communication of cells
Hormones, Cytokines, immune system functions
Cytokines
Chemicals released by any immune cells, NOT antibodies
Ex: Histamine
Components of CVS
Heart, Blood, Blood vessels
Blood vesseles
Arteries, arterioles, capillaries, veins, venules
2 loops of the CVS
Systemic circulation
Pulmonary circulation
Systemic circulation
Blood flows from heart to tissues back to heart
Left heart
Pulmonary circulation
Blood flows from heart to lungs back to heart
Right heart
Difference between arteries and veins
An artery carries blood away from the heart
Vein carries blood TO the heart
What is special about renal and digestive circulation
They have 2 capillary beds instead of 1 (Portal system)
Pressure Gradient
A difference in pressure
It dictates how blood move through the body. Moves from high to low pressure
What happens to pressure as blood travels away from heart
The mean blood pressure decreases the further you move
Where is pressure greatest in CVS
Aorta
Where is pressure lowest
Vena Cava
Why does pressure decrease over distance?
Resistance
What provides resistance in CVS?
“things” in the blood, running into these things, walls of vessels, diameter of vessels
Important relationships of behavior of fluids and gas in CVS
Pressure, flow, and resistance
Pressure
The force exerted by the fluid or gas on its container
Units: mmHg
2 components of pressure
Dynamic and lateral
Dynamic pressure
Flowing components that is kinetic energy
Lateral pressure
Represents potential energy exerted on the walls of the system (still tech. KE)
Hydrostatic Pressure
Energy that is exerted on the walls of blood vessels (lateral movement/pressure)
Use Hydraulic instead because it is not “static”
Friction in CVS
The farther the fluid has to flow, it will lose energy due to friction
Sources: blood vessel walls, cells within blood rubbing against each other
What creates pressure in the CVS
The heart
As it contracts it creates the driving pressure
Flow depends on…
Pressure gradient
Only flows if ∆P is positive
Flow is directly proportional to ∆P
aka higher gradient = higher flow
does NOT depend on absolute pressure
Resistance (R)
Forces which reduce the flow of blood
Flow ∝ 1/∆R
Parameters that determine resistance
radius of vessel (r)
length of vessel (L)
Viscosity, thickness of blood (fancy n)
Poiseuille’s Law
R = Ln/r^4
Resistance increases as length of vessel and/or viscosity increases
Resistance decreases as radius increases
Why is radius of vessel considered the most important factor in providing flow resistance
Length of vessels is constant
Viscosity can change but it takes time
So, changing radius is the most common change that will effect resistance
So, really R = 1/r^4
Vasoconstriction
decrease in diameter
Vasodilation
Increase in diameter
Larger radius implies
Less resistance
Flow equation
Flow ∝∆P/R
Flow Rate
Volume of blood over time (L/min)
It’s how much is going through
Flow higher in large blood vessel
Velocity of flow
the speed at which blood flows
Velocity higher in small blood vessel
General heart anatomy
~ size of fist
inverted cone with apex (tip) pointed down
Encased in pericardium
4 chambers- R&L atria, R&L Ventricles
Pericardium
tough membranous sac with clear pericardial fluid (lubrication to prevent rubbing/friction)
Pericarditis
Inflammation of pericardium, increases rubbing
Myocardium
composes 99% of heart
Covered by thin epithelial and connective tissue layer
2 Largest veins
Superior and inferior vena cava
General flow of blood in heart
Through Vena cave to RA
Through right AV valve (tricuspid) to RV
Through pulmonary semilunar valve to lungs
Into LA via pulmonary veins
Through left AV valve (bicuspid) to LV
Through aortic semilunar valve out aorta
Atria
Receive blood from vena cava or pulmonary veins; smaller chambers, thinner walls
Ventricles
Pump/eject blood into the aorta or pulmonary artery; larger chambers, thick walled
LV larger than right because pressure in aorta is very high and must be overcome by LV to pump blood through it
Common aortic (systolic) pressure
120 mmHg
Purpose of valves
Prevent backward flow of blood
Atrioventricular valves (AV)
B/w atria and ventricles
Tricuspid- RA:RV
Bicuspid (mitral)- LA:LV
Semilunar valves
B/w ventricles and their arteries
Aortic- LV:Aorta
Pulmonary- RV:pulmonary trunk
Prolapse
Regurgitation of blood b/c valve in wrong place
Stenosis
valves don’t open fully (less blood flow)
Incompetent valve
valves don’t close (reduces pressure)
Artesia
Valves don’t form properly
Chordae tendinae
Collagenous tendons that connect AV valves to cardiac muscle
Papillary muscles
Extensions of ventricular muscle
Stabilize chordae tendinae, DONT actively open/close valves (pressure does that)
How AV and semilunar valves open/close together
Ventricular contraction pushes blood against: AV valves causing them to close and chords prevent prolapse and semilunar valves causing them to open and blood exits ventricle
Coronary circulation
Provides blood to heart, different anatomically in everyone
Cardiac muscle uses 70-80% of O2 delivered to it, twice as much as other tissue because of high metabolic demand
Widowmaker
Anterior interventricular branch of LCA (LAD)
B/c controls bloodflow to so much myocardium
Primary cardiac muscle cell
Contractile cells (myocardium)
Smaller, branched, single nucleated
Adjacent cells joined by intercalated disks
Rely Less on extracellular calcium entry and more on intracellular stores
1/3 cell volume = mitochondria b/c of metabolic demand
Intercalated disks
Join adjacent cells
made of desmosomes (cell-cell junction) and gap junction (control ion/molecule movement)
Pacemaker cells (autorythmic)
remaining 1%, set the HR (HR can be altered by autonomic nervous system and hormones)
generate action potentials on their own
Concentrated in Sinoatrial node and AV node and bundle branches
HR #s to know: Resting, No Autonomic NS, AV node only, branches only
Resting 60-75
No Autonomic 90-95
AV node only 50-60
Branches only 30-45
Default HR is fastest pacemake (SA)
EC-Coupling of contractile cell
- Action potential enters from adjacent cell, flows down T-Tubule
- Voltage gated Ca channel opens, Ca enters cell
- Ca induces Ca release from SR via RyR
- Release causes Ca spark
- Summed sparks create Ca signal
- Contraction of sarcomere like skeletal from here
Differences in Contractile cell vs skeletal EC- Coupling
No neuromuscular junction
Intracellular Ca more important in cardiac
Ca channel not attached to RyR in cardiac
Relaxation in cardiac also includes Na-Ca exchanger (NCX)
Similarities and differences between Myocardial contractile cell Action potential and skeletal muscle cell
Similarities: Na+ entry and K+ exit
Differences: Repolarization is delayed (plateau), resting membrane potential is -90mV instead of -70mV
AP of contractile cell is much longer (~20x)
Myocardial contractile cell AP
- voltage gated Na+ channels open (voltage comes via gap junctions)
- Na+ channels close at peak (+20mV)
- Ca channels open, Ca enters cell and keeps mp high, fast K channels close
- Ca channels close and slow K channels open, mp decreases
- Resting potential reached, no overshoot and hyperpolarization
Ion channels in myocardial contractile cell vs. neuron/skeletal muscle
Same Na channels
Dif K channels
Add Ca channels
Why do contractile cells have plateau
Gives time for blood to fill the chambers while the heart is relaxed
Refractory periods of skeletal cell vs. contractile
Skeletal refractory periods are very short and can occur multiple times very quickly. They can be summed to reach max tension
Contractile cells have long refractory periods so a second AP can’t be fired until heart is relaxed and filled. NO summation
Why use 220 to calculate max HR
It is about the time it takes for one refractory period which means that is the fastest the heart can contract
why are Autorhythmic cells the pacemakers
Unstable membrane potential provide pacemaker ability
Have Pacemaker potential not resting membrane potential
If channels (funny channels)
Permeable to both Na and K to create current
more NA going in than K out
Slow depolarization (like drip faucet); speed variable
Close once threshold is released
Ions responsible for rising and falling face of autorhythmic AP
Ca entry is responsible for rising (instead of Na)
K exit is still responsible for falling
General AP of Autorhythmic cell
Start around -60 mV (approx bc unstable0
1. Slow drip via If channels until threshold (-40 mV instead of -55mv) is reached
2. Ca enters via voltage gated channels, If are closed
3. Ca channels close, K channels open
4. Once return to -60mV K+ channels close and funny open again
Why no hyperpolarization in autorhythmic cells?
The funny channels open back up again at -60mV preventing it from happening
Can you recreate table 14.3 (slide 44)
Go do it!
Sinoatrial Node (SA)
main pacemaker of heart; connected to AV node via internodal pathways
How does electrical signal spread through heart
SA node –> AV node;
Purkinje fibers, AV bundle, bundle branches
Contraction wave follows electrical signal wave
Order of depolarization/electrical conduction
- SA node depolarizes
- Electrical activity goes rapidly to AV node via internodal pathways
- Depolar spreads more slowly over atria, conduction slows through AV node
- Deplar moves rapidly through ventricular conducitng system to apex
- Depolar waves spreads upward from apex
Direction of contraction for atria and ventricles
Atria contract down
Ventricles contract upward to push blood out aorta/pulmonary vein
AV node delay
Atria must complete contraction before ventricles begin, so conduction is slightly slower
Bundle branch block
Ventricle contraction is not simultaneous
1st, 2nd, and 3rd degree heart block
Signals don’t reach AV node correctly
Long-QT syndrome
Ventricular contraction and relaxation are delayed
If default HR is fastest (SA 90 bpm) why is resting HR 60-70 bpm
Autonomic nervous system; Parasympathetic
Basics of Electrocardiogram (ECG/EKG)
Electrical activity of heart follows a pattern; SUMMED electrical activity of ALL heart cells; basic requires 3 leads (both arms, left leg)
Interpretation of EKG depends on
Direction electrical wave travels (atrial/vent)
Type of electrical wave (dep/rep)
Whether the lead is positive or negative
What charge do depolarizing and repolarizing waves have
Depolarizing: Negative
Repolarizing: Positive
2 ways to get positive deflection
Depolarizing moving TOWARDS positive electrode
Repolarizing moving AWAY from positive electrode
3 major components of ECG
Waves, segments, intervals
Waves
Part of ECG trace that goes above/below baseline
Segments
Sections of baseline between waves
Intervals
Combinations of waves and segments
P -Wave
Atrial depolarization
QRS complex
Ventricular depolarization; hides atrial repoalrization
T wave
Ventricular repolarization
Can u read an EKG?
Go do it. slide 55
PR Segment
Conduction through AV node and AV bundle
Diastole
Cardiac muscle relaxing; chambers are filling with blood
Systole
Cardiac muscle is contracting; chambers are ejecting blood
Time heart spends in systole vs diastole
2/3 time in diastole
Late diastole
Both sets of chambers are relaxed and ventricles fill passively, pressure higher in atria, AV valves open
Atrial Systole
Atrial contraction forces a small amount of additional blood into ventricles (complete ventricle filling); quick
Heart sound 1
After Atrial systole; closing of AV valves because blood pushes back on them
Isovolumic ventricular contraction
1st phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. Max ventricular blood volume (EDV)
All 4 valves closed
Ventricular ejection
As ventricular pressure rises and exceeds pressure in the arteries, semilunar valves open and blood is ejected
Heart sound 2
Dup, Closure of semilunar valves, end of ventricular systole
Isovolumic Ventricular relaxation
As ventricles relax, pressure in ventricles falls. Blood flows back into cusps of semilunar valves and snaps them closed. Minimum blood volume in ventricles (ESV)
All 4 valves shut
Pressure Volume loops
WORK THROUGH DIAGRAM slide 62
Stroke volume
EDV - ESV = SV
The amount of blood pumped out by one ventricle during contraction
Not all blood ejected for safety margin
More forceful contraction = more blood ejected
Ejection fraction
Another way to look at stroke volume;
Percentage of EDV ejected (ESV/EDV)
Normal heart health is 50-70%
Cardiac output
The volume of blood pumped by one ventricle in a given period of time (L/min)
Measures heart performance and indicator of total blood flow through body
CO = HR * SV
Under autonomic and endocrine control
Typical is about 5 L/min
Wiggers Diagram
Go through it. lol yikes
Sympathetic activity on heart
Increase HR (faster depolarization)
Catecholamines increase ion flow of If (Na) and Ca channels
Bind B1-arenergic receptors on autorhythmic cells, increase cAMP
See diagram slide 70
Parasympathetic activity on heart
Decrease HR
Acetylcholine release binds muscarinic cholinergic receptors
Increase K permeability but decrease Ca permeabaility (doesn’t mess with Na)
Delay depolarization in autorhythmic cells
See diagram slide 70
Tonic control of HR
Balance, not like a light switch, not either/or
Parasymp dominates at rest
Symp dominates during exercise/stress
Preload
How much blood fills the ventricle before contraction
Dictated by venous return (blood entering RA); diastolic
Increase preload, increase SV
What dictates venous return
Skeletal muscle pump
Respiratory pump- thorax movement
Sympathetic constriction of veins
All increases preload
Afterload
Mean pressure in aorta
The higher mean arterial pressure the harder LV has to work to eject blood
Increase afterload–> decrease SV
Leading cause of heart failure
Contractility
intrinsic ability of cardiac muscle fiber to contract at any given length
Increase contractility –> increase contraction force (more Ca entry)
Force is Ca dependent
Inotropic agents
increase or decrease force of contraction (more/less SV)
Catecholamines increase contractility
Other chemicals decrease
Heart length-tension relationship
Increase length –> increase filling –> increase SV
Only to a point
Frank-Starling Law
EDV and SV are proportional
Within limits (pericardium sets to prevent too much stretch) heart pumps all blood that enters it
Plateau on graph
Cardio calcs + output
Go through slide 77!!! and calcs on blackboard/pic
General blood vessels composed of
Smooth muscle
Connective tissue (elastic and fibrous)
Endotherlial cells (endothelium)
One features all blood vessels share?
Endothelium
Composition of artery
Endothelium, elastic tissue, smooth muscle, fibrous tissue
Composition of arteriole
Endothelium, smooth muscle
Composition of Capillary
Endothelium
Composition of venule
Endothelium and fibrous tissue
Composition of vein
Endothelium, smooth muscle, elastic tissue, fibrous tissue
Smooth muscle on blood vessels
Controls vasoconstriction and dilation; tonic constriction
Ca-dependent
Small vs. large arteries
thick and elastic, difficult to stretch, smaller arteries are more muscular
Arterioles
Major site of resistance
Diameter changes due to smooth muscle
Metarterioles
bypass capillary beds which reduces flow to tissue
Capillaries
Regulate exchange, smallest of all vessels
Lack SM and elastic/fibrous tissue
Flat shape helps exchange
Permeability varies by need
Venules
Similar to capillary
convergent in appearance
SM appears in large ones
Veins
Thin, large vessels with one way valves
Skeletal muscle pump and respiratory pump aid flow
Skeletal muscle pump
Aids blood flow in veins
When muscle contracts it compresses the veins and forces blood toward the heart
What creates blood pressure
Driving pressure: L. vent ejects blood to aorta, aorta expands to accommodate CO, elastic recoil propels blood forward
Obeys fluid flow (pressure gradient)
Arterial pressure is pulsatile (elastic recoil)
Venous pressure is steady
Diastolic pressure
Aortic pressure during ventricular diastole
Healthy 60-80
Systolic pressure
Aortic pressure during ventricular systole
Healthy 100-120
Pulse pressure
PP = systolic - diastolic
Mean arterial pressure calculation
MAP = diastolic + (1/3)(PP)
MAP = CO * Rarterioles
with CO = HR*SV
Venous pressure
Approaches 0 in the Vena cava
Pulmonary pressure
Exists, we will cover later
Mean arterial pressure
Closer to diastolic pressure because it is longer
Measured with sphygmomanometer
Low MAP
tissues receive less gases and nutrients
High MAP
Blood vessel rupture
Causes heart to pump harder (high afterload)
Blood vessels get thicker and stiffer which increases resistance
Capillary damage
Mechanisms that alter arteriole resistance
Local Control- metabolism, paracrines, auto regulation
Sympathetic reflexes- restrict flow to organs, determine blood distribution
Hormones- regulate salt/water excretion, regulate autonomic reflex control
Chemicals that mediate vasoconstriction
Norepi, vasopressin, Angiotensin II (most prominent)
Chemicals that mediate vasodialation
Epi, Nitric oxide (most potent)
Myogenic autoregulation
Local control of flow
Form of self regulation
Increase in BP –> Increase flow –> Increase SM stretch, vessel then constricts on its own to maintain balance
Strong in brain and kidneys because they need steady, constant blood supply
Metabolism as Local flow control
Low O2 and high CO2 at arteriole dilates arterioles
Increased flow provides O2 and removes CO2
Active hyperemia
Active Hyperemia
Increased blood flow in response to increased metabolism
Occlusion of BV (local control)
Blockage leads to waste accumulation and O2 falls
Endothelial cells produce Nitric oxide (dialator)
When flow resumes, significant vasodilation occurs to clear out waste
Reactive hyperemia
Vasodilation in response to low perfusion
Similar to active hyperemia but the trigger is different
How is the trigger different between reactive and active hyperemia
In active an increase in metabolism triggers dilation
In reactive the dilation follows a period of decreased blood flow
Sympathetic control of vascular smooth muscle
Most arterioles innervated by sympathetic neurons
Norepi bind alpha receptors which causes CONSTRICTION
Dilation achieved by decrease in norepi release
EXCEPTION: arterioles of heart, liver, and skeletal muscle respond to Epi
Epi causes DILATION by binding to B2 (don’t want to constrict these arteries)
Brief receptor effect summary
B1 on heart –> increase HR, and Ca entry
B2 on BV –> Vasodilation
alpha1 on BV –> vasoconstriction
Why is there no parasympathetic dilation if sympathetic mostly constricts arterioles?
It would create too quick a drop in BP if parasymp could immediately dilate after constriction by symp.
Blood distribution
Unequal in body, changes with movement/position
More important organs get more blood per mass unit even if they get less overall quantity of blood
Resistance determines path of flow
Blood wants to take path of least resistance, so if there is some form of resistance it will deviate itself to go somewhere else
What blood flow is almost constant?
Cerebral and renal
Stays constant even in stress/exercise because strong myogenic autoreg
Coronary flow regulation
Exception
Depends on heart activity level
Myocardium release adenosine which causes coronary dilation
*not myogenic autoreg.
