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- University of Michigan - Ann Arbor
- Medicine
- Medicine 102
- Rust
- Physiology Unit 2 (Everything in One Lonnnnng Note :) )
Physiology Unit 2 (Everything in One Lonnnnng Note :) )
Medicine 102 with Rust at University of Michigan - Ann Arbor
About this deck
By: Erika B.
Created: 2011-02-19
Size: 108 flashcards
Views: 16
Created: 2011-02-19
Size: 108 flashcards
Views: 16
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Smooth Muscle
general function is to move contents of tubes/ organs
(via contraction/ change in diameter)
- spindle shaped
-no striation / parallel sarcomeres
Smooth compared to Skeletal
SIMILAR: Length Tension relationship, Max. tension per unit cross sectional area, in both oxidative fibers weaker than glycolytic
DIFFERENT: Smooth can develop tension over larger range of lengths[these muscles are constantly stretching to fill and contracting to release],
(however as a single cell, smooth can develop less absolute force)
Smooth Muscle Thick/ Thin filaments:
one of the Myosin Light Chains on the neck of the thick filament is the site of contraction regulation
How is Smooth Muscle Contraction Activated by Ca2+
regulated by cytosolic Calcium (like in skeletal) but action of Ca2+ is more sig.
^Ca2+ , binds to protein Calmodulin, Activation of Ca-cal. myosin light chain kinase: phosphorylation of MLC, cross bridge cycling
ATP utilization: lower than skeletal muscle
shortening velocity is slower ^
fatigue resistant
Cross Bridge Cycle (Smooth) [tension n shortening]
other than the attatchment step: same as Skeletal
The energized cross bridge (with ADP +PO4 bound to head) interacts with actin- power stroke occurs( due to release of PO4 and ADP )> ATP binds to detach the cross bridge > hydrolysis of ATP re-energizes the head and crossbridge cycling can occur again, AS LONG AS THE PO4 IS STILL BOUND TO THE MLC.
Relaxation (Smooth)
Ca2+ levels decrease: less MLCK active: MLC phosphatase dominates (dephosphorylated
How is Ca2+ removed from the cytosol
ATPase on plasma membrane
Ca2+- Na+ exchanger on the plasma membrane (Na+ gradient is energy source)
ATPase on SR membrane
Calcium into Smooth Muscle:
can come from ECF (calcium channels on plasma membrane) or SR (calcium channels on this membrane: opened by second messengers)
Signals for Activating Smooth Muscle
*one input: the Motor neuron (release of ACh is always excitatory (cause of contraction) )
>>> Membrane depolarization: AP may be generated, but not necessary.
>>> Chem. Messangers (such as Hormones, Paracrine Factors, Neurotransmitters, and Local Metabolites): can excite or inhibit
>>> Stretch: mechanical changes may cause Ca2+ channels to open: causing contraction.
Smooth Muscle Activation and Inhibition
1. A change in membrane potential will initiate Contraction by Opening of V-gated Ca2+ channel on the plasma membrane.
2. ligand gated Ca2+ channels: G-protein activated by messenger molecule to membrane receptor> opening or closing of these channels = mediated
Smooth Muscle Activation/ Inhibition continued
3. Opening of Ca2+ channels on SR without AP: Binding of a messenger molecule to a membrane receptor activates a G-protein mediated 2nd messenger cascade that generates IP3 and IP3 will gate the SR Ca2+ channel open.
4. Stretch activated channels: (contraction to oppose the stretch) Alternately, decreased stretch will close these channels and lead to relaxation of the fibers.
Action Potentials
smooth muscle cells do not utilize V-gated Na+ and K+ channels to generate AP
Depolarization is due to Ca2+ influx!
*slower rate of Dep. and Rep. has a lower peak amp.
Pacemaker Potential (Spontaneous Electrical Activity)
*only certain cells, no stable resting Vm*
A: Ca2+ dependant K+ channels close and the membrane depolarizes B: Voltage-gated Ca2+ channels open and AP occurs, cytosolic Ca2+ rises C: Ca2+ dependant K+ channels open and membrane hyperpolarizes D: V-gated Ca2+ channels close and cytosolic Ca2+ decreases
Closer look at the Pacemaker Steps : A
Originally @ most hyperpolarized state, Ca2+ dependent K+ channels close, membrane depolarization due to decreased K+ efflux
Closer look at the Pacemaker Steps : B
Depolarization to threshold opens Ca2+ channels. Ca2+ levels in cytosol increase
Closer look at the Pacemaker Steps : C
Ca2+ interacts with Ca2+ dependent K+ channels which reopen. Membrane repolarizes (hyperpolarizes)
Closer look at the Pacemaker Steps: D
Ca2+ channels close/ cytosolic Ca2+ levels decrease leading back to step A
Pacemaker Cells
Connected to nearby/adjacent non-pacemaker smooth muscle cells by Gap Junctions
WHICH aid in speed, increase cell synchronization, are bi=directional...
Single Unit Smooth Muscle
1.Contain pacemaker cells
2.Connected by gap junctions
3.Synchronous activity
4.Activity altered by inputs (ie. autonomic innervation near/ circulating hormones/ paracrine factors) to pacemaker cells
5.Contraction can be initiated by stretch
---Examples: GI, uterine and small diameter blood vessel smooth muscle.
Multiunit Smooth Muscle
*individual cells are separate from each other...
Few or no gap junctions 1.Activity is not synchronous- APs not utilized to generate force
2.No pacemaker cells 3.(Autonomic neurons= extensive)Richly innervated throughout the muscle
4.Not responsive to stretch
5.Contractions often do not require AP’s in the membrane
6.Examples: Airway and large artery smooth muscle
Cardiovascular System
for molecule transport over large distances (between in and external environments)
REMINDER:
extracellular fluid: plasma and interstitial fluid
Components of Blood:
Plasma: contains dissolved nutrients, proteins, metabolic wastes, ions, gases, and hormones
Leukocytes: immune cells
Platelets: cell fragments involved in clotting
Red Blood Cells: Transport of O2 and CO2
Basic Components of the Heart
Right Atrium > Right AV (tricuspid) valve> Right Ventricle> Pulmonary semilunar valve
Left Atrium> Left AV (bicuspid) valve> Left Ventricle> Aortic semilunar Valve
Remember:
from sup/inferior vena cava: flows thru the RIGHT side> blood exits to pulmonary artery (WHICH CARRIES DE-OXYGENATED BLOOD) * pulmonary circulation (lungs...)
PULMONARY VEIN carry's OXYGENATED blood back to LEFT side> blood exits thru Aorta: *Systemic circulation
Termsss
HR= beats/ min (70 at rest)
*SV= ml/ beat (volume ejected from each ventricle simultaneously) (70 at rest)
*CO= L/min (volume ejected from each ventricle simultaneously) (5 at rest)
*VR= Amt. of blood returned to ventricle per minute (same as cardiac output) (5 at rest)
* so remember, this is per ventricle not overall!!! :)
order of stuff
arteries
arterioles
capillaries
venules
veins
*systemic: arteries are oxygenated, veins are deoxygenated
*opposite in pulmonary!
Bulk Flow
driven by a pressure gradient
<3 = the pump that provides the pressure to drive flow
p1> p2 = ------> forward flow
Relationship between F, R and P is direct!!!!!!!!! woooooo
Radius and Resistance
Flow rate= Pressure Difference/ Resistance
* in our circ. system: resistance is primarily due to blood vessel radius
Radius is proportional to 1/r^4..... (confused?? this means ^!!!)
Poiseuille's Law
*** MAP = CO x TPR = HR x SV x TPR
The homeostatically regulated variable in our cardiovascular system is MAP
Hematocrit
Percentage of blood that is red blood cells
** increased hematocrit increases viscosity:: resistance!
How can we increase the flow of blood through a tube
decrease the Resistance (increase the radius)
increase the pressure
Efficient Pumping of the <3 Requires:
Synchronized (non- arrhythmic) Contraction
Forceful (not failing) Contraction
Valves fully open (not stenotic)
Valves do not leak (aren't insufficient)
Fill adequately
Cardiac Pacemaker Cells
Like those of smooth muscle, are connected to nearby non-pacemaker cardiac muscle cells by gap junctions
synchronized, forceful contractions
Conducting System of the <3
Pathway of Depolarization
AV node is the only connection between atria and ventricle for AP conduction
*Atrioventricular (AV) Node: 50 AP/min
*Bundle of His:25-40 AP/min (right and left branches)
*Purkinje Fibers : transmit AP's at 1.5-4 m/sec
SA Node AP (order)
Slow Depolarization: F-type open (NA+ in), V-gated close (K+ "trapped!")
Rapid Depolarization> Action Potential : T-type open/ inactivate (Ca2+ in), L-type open (Ca2+ in)
Repolarization/ Hyperpolarization: V-gated open (K+ release), L-type close (no more Ca2+ in)
Sequence of Cardiac Excitation
Spontaneous SA node AP generation (no input)
*fastest pacemaker: can depolarize the others early!
Electrical activity leads to contractile activity
wave of repolarizations are in the opposite direction!
*see piccc
Ventricular Muscle Fiber AP :: generation of force
V-gated Na+ open (depolarization thru gap junctions) *quick like skeletal muscle*
V-gated Na+ inactivate
L-type Ca2+ open due to initial depolarization, V-gated K+ channels close
Different V-gated K+ open (these are delayed), L-type Ca2+ close (b/c of repolarization *refractory period is longer*)
blahh blahh :)
A closer look at the Calcium-Induced Calcium Release:
Ca2+ influx from the ECF:
-Maintains depolarization (longer refractory period): NECESSARY IN <3 FOR FILLING UP WITH BLOOD!
-Causes release of Ca2+ from SR
-Is required for forceful contraction
Cardiac Muscle Relaxation
SERCA, the Ca2+-ATPase on the SR membrane
Na+-Ca2+ exchanger on the sarcolemma (plasma membrane)
Ca2+ is removed to ECF or SR (and as Ca2+ levels drop, relaxation occurs just like in skeletal muscle
Electrocardiogram (ECG)
Detects current flow/ <3's electrical activity
*excitation= depolarization: precedes contraction
P- Atrial excitation
QRS- Ventricular Excitation
T- Ventricular repolarization (precedes relaxation)
Intervals (and segment)
p-q interval: AV node conduction time
q-t interval: Ventricular contraction time (systole)
t-q segement: ventricular relaxation time (diastole)
r-r interval : heart rate
HEMOSTASIS: Blood Coagulation!!! AKA clot/ thrombus
overview of process: filamentous protein fibrin traps red blood cells and platelets
-stops blood loss from a ruptured vessel
-positive feedback cycle: extremely rapid
Problems of Hemostatis
Hemophelia: no clotting factor :(
low platelet counts
pooling (when no injury!)
occurrance when or where it should not? can lead to stroke, <3 attack, or embolism!!!
Physiological Hemostatic Mechanisms
Immediate/ inherent response: vessel constriction to reduce blood flow and loss
*vasoconstriction
Formation of a platelet plug (initiates clotting)
Blood coagulation (^dependent--- rapid succession)
In AND Extrinsic factors!!!
Platelets
fragments of megakaryocytes
always circulating (inactive)--- activate upon exposure to certain factors
so how do platelets become active?
exposure to collagen!
activated platelets become sticky and aggregate: release chemicals to increase this response (thromboxane A2)>> platelet plug!
More specific look at clotting
Platelets adhere to collagen
receptors for fibrinogen are exposed/activated, secrete TXA2 as a pro-plug formation factor
aggregation
compression/strengthening
undamaged epithelium secrete Nitric oxide (NO) and prostacyclin (PGI2) to inhibit aggregation on healthy vessel portions!
How are platelet plugs localized to damaged area?
undamaged cells are releasing anti-aggregation factors :)
- nitric oxide and prostacyclin
Silly Similarities in Platelet Factors:)
Thromboxane A2 and Prostacyclin are both cox inhibitors?
formed verrrrry similarly : originally aracadonic acid.... etc... basically they are similar except for their final structure, which determines whether they activate or inhibit aggregation
Liver's Role
Vitamin K Absorbtion and synthesis of Clotting Factors
Key Points of Clotting Cascade
Inactive precursors circulate in blood
exposure to underlying tissue (bc of damage)
Inactivators: factors that limit clot formation
Thrombomodulin (inactivates Thrombin) (activates protein C)
Protein C (inactivates 5a and 8a)
Antithrombin 3 (interacts with heparin to inactivate thrombin)
* if 5 is not inactivated: remains pro-clotting!
Fibrinolytic System: Breaking up an existing clot
presence of a tissue plasminogen activator (t-PA) [secreted by endothelial cells]
activated by binding w. fibrin
activates plasminogen to plasmin: fibrins broken down
Ewww Coronary Artery Disease :/
lipid-rich core of plaque...wall breaks ...clot forms... blood flow stops... muscle cells die (myocardial infraction: <3 attack)
Clotting Disorders
Thrombocytopenia (decreased platelets)
Hemophilia -OR-problems with liver/vitamin K (decreased plasma clotting factors)
Thrombophilia (increased clotting)
Cyclooxygenase's role in clotting
enzyme involved in production of TXA2 from arachidonic acid (and prostacyclin production too!)
inhibition of this= less TXA2, and less platelet activation: reduced chances of clot formation
PGI2 doesn't work the same bc it is made by endothelial cells (has nucleus and can make more cyclooxynase to replace inactivated enxyme)
Anticlotting Drugs
Aspirin
Anti-vitamin K drugs
Fibrin Dissolving Drugs
Heparin
Systole
Part of the cardiac cycle which refers to isovolumetric ventricular contraction and ventricular ejection
*blood flow out!
(Aortic and Pulmonary valves open only)
Diastole
Part of the cardiac cycle which refers to isovolumetric ventricular relaxation and ventricular filling
*blood flow into ventricle
(AV valves open only)
What changes during the cardiac cycle?
Pressure, Volume, ECG and Valve
What causes the sound during a heart beat?
The closing valves (pressure)
1st: AV valve closing (start of systole)
2nd: Pulmonary/ Aoritc valve closing (start of diastole)
Pressure Changes
(looking specifically at the left side in all of these examples)
atrial pressure stays relatively the same
ventricular pressure = below atrial in diastole moments, but in systole: SPIKES
aotic pressure= pretty high, spikes in systole (diotic notch @ very beginning of diastole, and then a gradual decline to "starting" pressure
Volume Changes
End Diastolic Volume (after filling: max)
Volume (obviously) drops during systole (end systolic volume= min)
Here's information that is pretty darn basic
The right side of the heart: "drives" pulmonary circulation, and all "right side blood" is deoxygenated.
The left side of the heart "drives" systemic circulation, and all "left side blood" is oxygenated
Systemic (acts in parallel) and Systemic AND Pulmonary circulation act in series
In other words Blood that enters pulmonary circulation is originally deoxygenated, gains oxygen, and is thus cycled systemically... etc.etc.
So why (in graph form.. and whatnot) is the Left side pressure change more varied? (aka. right side of heart: pressure is much lower in general)
The right side doesn't need to generate as much force as the left...(which has a thicker ventricular wall)
(although, there is an identical cardiac output/flow.. therefore: we can deduct that Pulmonary Resistance is Lower than Systemic Resistance)
>>> One difference???: Right atrial pressure drops below right ventricular pressure DURING ISOVOLUMETRIC CONTRACTION (av-valve close) [as opposed to during vent. ejection phase like on the left)
Stenoic Vs. Insufficient Valve (MURMURS)
Stenoic= Narrowed valve (when open) >> Turbulent Flow
Insufficient= Leaky valve (when closed) >> Turbulent Backflow
*murmurs are not usually an issue if there is no significant change in stroke volume.
Diagnosing a murmur
heard during systole: (right after 1st sound)
Aortic/ Pulmonary Stenosis, AV valve Insufficiency
heard during diastole: (right after 2nd sound)
Aortic/Pulmonary Insufficiency, AV Stenosis
Regulation of Heart Rate and Stroke Volume
CO <Liters per minute produced> = SV<determined by force contraction of ventricle> x HR <determined by rate of SA node>
^direct influence on one another.
Autonomic Innervation of the <3
Vagus nerve (PARASYMPATHETIC): stimulates SA and AV nodes *specifically to pacemakers (?) ---------effects Heart Rate (opposite) :: ^ para, decrease HR
SYMPATHETIC cardiac nerve: stimulates SA and AV node, and Ventricular myocardium(muscle) ----------effects both Heart Rate and Stroke Volume (directly)
Autonomic Innervation Simplified!
Parasympathetic activity releases ACh, and thus reduces Heart Rate
Sympathetic activity releases Nor-Epi, and thus increases Heart Rate
ANOTHERRR look at the Autonomic Innervation
Control of HR: via changes in
1. symp. activity (increases permeability to Na and Ca> more influx)
2. parasymp. activity (increased permeability to K > more efflux) (also reduces permeability for Na and Ca)
3. Circulating Epinephrine levels
Control of SV via
1. Changes in symp. activity (increases contractility)>> expression of beta adrenergic receptors
2. The Frank-Starling Mechanism (Starling's Law of the Heart)
(shows us that ^ symp. activity, no matter the EDV, ^ contractility):: ^EF
Ejection Fraction
Symp activity.. increases contractility.. contraction occurs with more force.. End Systolic Volume change (from End Diastolic Volume) is greater, Stroke Volume ^
EF=SV/EDV : aka. with increased contractility, EF increases.
Another look at Symp. Activity Effect on Force Contraction
3 things different between the two ventricular muscle twitch tracings
-shorter rate of contraction (duration) (b/c of Nor Epi.) -faster rate of relaxation (b/c of ^ Ca2+ removal, and lowered affinity of troponin for Ca2+) -greater peak tension (b/c of cytosolic Ca2+ increase-- more open channels)
Effect of Epi/ Norepi on Ventricular Muscle Cell
Activates cAMP- dependent protein kinase
- Ca2+ channels Open> more Ca2+
- Increases cross-bridge cycling
- Increases rate of ATPase activity
Overall Effect of Increasing HR
More blood in systole, less in Diastole (less fill)
under sympathetic activity, contraction and relaxation is completed more quickly to allow for more filling time
Frank Starling's Law of the Heart
(different mechanism to alter SV... not about contractility)
*** this is like the basic curve, not looking at the effect of symp. activity.
What this says is that an increased EDV (fill), leads to an increased Stroke volume
thus: ^ symp. activity :: decreased VR:: ^ cardiac filling, and CO
LAW: ^ EDV = ^SV
Cardiac Muscle Length-Tension Relationship
Stretching of cardiac fibers ^ the amt of tension generated
(stretch of ventricles during fill results in a more forceful ejection of blood)
^ cardiac fiber length = ^ tension
(to a point!! (optimal level)
Starling Overview
•SV^ as EDV^
•At any given HR, an increase in VR* will increase CO
–Increased VR → increased EDV → increased stretch of cardiac fibers → increased force of contraction → increased SV → increased CO
How can VR be altered?
change venous pressure
(either by ^ PVP or decreasing CVP, or the Addition of volume of fluid/ constriction of veins)
How can Venous Pressure (or EDV) be altered
directly (both) by
Sympathetic activity, skeletal muscle (contractions) pump, Inspiration depth(respiratory pumps), or blood volume
*an increase in any one of these things will increase the following: VP, VR, Atrial Pressure, EDV, and CO
How does a skeletal muscle pump increase VR?
normally, venous circulation is low pressure (see, this is why the VEINS have valves: to prevent back-flow!
contracted muscle narrows the vein, so pressure is raised: net flow= forward
How does a respiratory pump increase VR?
Thoracic and Abdominal Cavity: with inspiration, thoracic pressure is lowered, but abdominal is increased.
This change in pressure between peripheral veins and heart leads to an ^VR (and blood flow to the heart)
Control of Cardiac Output (Summary)
^ EDV, ^ symp. activity (increase epi), Decrease parasymp. activity,
*with these all we see increased <3R and increased SV
Will increase CO*** quick review: CO= ml/min, SV= ml/beat, HR= beat/min***
Parts of a Blood Vessel
Connective Tissue (adventitia), Vascular Smooth Muscle (media), Connective Tissue (intima/ internal elastic lamina), Endothelium, Lumen (blood flow)
Arteries
Pressure reservoirs
Very elastic (stretch but recoil)
^stretch to maintain flow/ pressure during diastole
Some smooth muscle Low and unchangeable Resistance
Some smooth muscle Low and unchangeable Resistance
MAP(93>> round to 100) is closer to diastolic pressure bc more time is spent in diastole
(120/80= systole/diastole)
Arterioles
Resistance vessels
Less elastic, more rigid Thicker smooth muscle layer Sympathetic innervation Resistance vessels High R and changeable R Changes in R alter MAP and organ blood flow
Tonic [myogenic tone]("regular (intermediate) size"- resting tone), contraction of smooth muscle (causing vasoconstriction (^R)) [neurogenic tone], Relaxation of smooth muscle (causing vasodilation (lower R))
Capillaries
Exchange vessels/ nutrients (thinnest walls)
Endothelial cell layer only
color change of blood: removal of oxygen from hemoglobin
total resistance is not very high: more exchange time
*arteriole dilation: Pcap increases*
Venules
Post-capillary Resistance Vessels (valves drive VR)
Thin layer of smooth muscle Distensible (less elastic in terms of recoil-- (don’t push back))can have valves Sympathetic innervation
(alpha receptors)
constriction increases PVP>>> increases VR and SV
Veins
Capacitance Vessels (holds a lot of blood at low pressure)
Very compliant (distensible) Thin layer of smooth muscle Have valves Sympathetic innervation ^ volume= ^P = ^VR =^ CO
60% of blood on v. side
changes in diameter are pretty small
SMALL CHANGES IN PVP= SIG AMT of VR
Arteriole Radius
Affected by the following factors:
Neural controls:
vasoconstrictors - sympathetic nerves
vasodilators- Nitric oxide release from nerves
Hormonal controls:
Epinephrine (diff forms dilate/constrict)
Local controls:
vasoconstrictors- internal blood pressure...
vasodilators- less o2, influx of K, CO2, H+, nitric oxide, substances released during injury, lower pH
Effect of changes in arteriolar diameter on MAP and capillary Pressure
dilated Arterioles (lower resistance)= lower MAP (pressure drop), increased cap. pressure (faster flow)
constricted Arterioles (higher resistance)=higher MAP (fluid backup!), decreased cap pressure
*like a hose*> pressure drives flow
Major controller of TPR = changes in/ of Radius
ARTERIOLES PROVIDE MORE THAN 1/2 the TPR
Radius is controlled by hormonal input, paracrine factors, sympathetic neural input, and changes in local metabolites)
How can Hormones (aka. Epinephrine) act as both vasoconstrictors and vasodilators?
Different tissues have different epi Receptors!
alpha receptor: constrict (most tissue)
beta receptor: (usual response) dilation (at least in low/ moderate epi amounts)
- example^ exercise
the rule of thumb we go with though is symp activity causes constriction
Types of movement across capillary wall
Diffusion (MOST IMPORTANT MEANS OF NET MOVEMENT OF NUTRIENTS...)
^O2 and glucose from blood to muscle, CO2 out!^
UltraFiltration (bulk flow driven by pressure diff)
(opposite= (re)absorption)^from plasma to interstitial fluid^
aka Outward movement; net filt occurs at arterial end, wile net absorb (inward movement) occurs at venous end
Exocytosis/Endocytosis (moves specific proteins)
daily fluid movement across caps
Ultrafiltration: 20 L/ day
Osmotic reabsorption: 17 L/ day
Lymph: 3 L/day (another form of returning ISF to plasma
Edema (swelling associated w. increased ISF volume)
Causes:
(^ ultrafiltration) due to ^ in Pcap
Decreased reabsorption
Disruption of lymph flow
Arterial Pressure is Homeostatically Regulated
MAP drives flow, and must be maintained to ensure adequate O2/nutrient delivery... and removal of CO2/ metabolic end products
MAP=COxTPR (SVxHRxTPR)
Receptors/sensors are the Arterial baroreceptors (carotid sinus and aortic arch)
MAP ^= Firing Rate ^... etc
effector tissues are conducting system (HR), cardiac muscle (SV) and blood vessel smooth muscle (TPR and VR)
Hemorrhage responses
Decreased blood volume causes:
decreased: VR, SV and CO
increased: HR
Arterial constriction (to increase the decreased Arterial pressure, and to decrease the capillary pressure)
*autotransfusion* reabsorbtion into caps to make up for lost fluids (dilute) (decreases ultrafiltration)
diversion of blood flow to maintain perfusion to heart and brain
via local controls: not via altered symp/ circulating epi... resistance doesn't change due to the hemmorage
but a Baroreceptor reflex (plays major role in blood pressure regulation in various situations)>
constriction on arterioles: and increased resistance to tissues. due to increased sympathetic and epi.
In the case of heart attack: what does a baroreceptor reflex do?
Immediate responses (not baro)
Decreased SV (CO)
Decreased MAP
HR increase
VR increase/ increased contractility
TPR increase
SV, CO and MAP increase (but not to normal)
Cardiovascular disease
Heart Failure (inadequate CO)
>> can be due to systolic (pump) fcn [cause: <3 attack/ arrhythmia]
or diastolic (fill) dysfunction [cause: hypertension]
Hypertension
chronically increased systemic arterial pressure
caused by ^TPR
Increases the afterload (pressure in arteries) on the <3
---- problem with this: high arterial pressure means ventricles musc contract w. more force, thus ventricular walls get thicker [hypertrophy]... WHICH CANNNN: decrease chamber size :( ((decreased EDV) (decreased SV...))
Coronary Artery Disease
insufficient blood flow to an area of <3 muscle (often caused by plaque in vessel wall/ narrowed lumen)
<3 attack can be caused by ruptured plaque/ formation of clot OR lodging of an embolism
*fix? angiography/plasty
If LV pumps less Forcefully than RV???
fluid backup in lungs! P^ (edema??)
Strenuous Exercise
^ CO, HR, SV, MAP, and lower TPR (due to vasodilation)
*MAP can be up bc of the elevated CO
Skeletal and Respiratory pumps aid in maintaining venous return (cardiac output) during exercise
** venous tone ^ due to ^ symp stimulation
control of CV system: increase of MAP by resetting Baroreceptor set point
Effect of Training:
On HR: decreased at rest and exercise, but no change in MAX rate
On SV: increased at rest and exercise due to moderate hypertrophy and increased chamber size (^ strength of contraction)
On CO: ^ MAX, no change @ rest
On Vo2 Max:^ with training (b/c of CO increase)
About this deck
By: Erika B.
Created: 2011-02-19
Size: 108 flashcards
Views: 16
Created: 2011-02-19
Size: 108 flashcards
Views: 16
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