Term
| functional differences between pulmonary and systemic circulation? |
|
Definition
| much lower pressure in the right system. it only needs to go to the lungs. the right system is much higher pressure because it needs to push blood to the entire body. |
|
|
Term
| the lymphatic system. what is its function? |
|
Definition
| accessory route for fluid balance. Often times with such a high pressure (left heart) system, you push a lot of water into the tissues. Some of it returns back to the venous system, but not all of it, so there tends to be fluid accumulation in tissues. the lymphatic system is the accessory route for these fluids back to the venous system. |
|
|
Term
| which ventricular wall is much larger, left or right? |
|
Definition
|
|
Term
|
Definition
| tricuspid and mitral (bicuspid) valves. prevent backflow from ventricles into atria. chordae tendinae prevent valve eversion with papillary muscles. |
|
|
Term
| what re the 3 layers of the heart? |
|
Definition
Endothelium – thin/inner, lines entire CV
– Myocardium – middle/muscle layer. contains myocytes - autonomic innervation - connected in series and branched. connected by intercalated discs (gap junctions and
desmosomes)
– Epicardium – thin/external
• squamous mesothelium/basal lamina
• blood/nerve supply within CT network. the coronary arteries lie in this layer, and then dive into the myocardium to supply it. |
|
|
Term
| what are gap junctions in the heart, and why are they there? |
|
Definition
| gap junctions allow ion flow (cytoplasm) between cells which allow an action potential to flow right through the whole heart. |
|
|
Term
|
Definition
| spot welds. keep the cells held together. |
|
|
Term
|
Definition
Pericardium – fluid filled sac
– Fibrous outer layer
– Inner secretory lining – pericardial fluid |
|
|
Term
| what are the 3 layers of most vessels? |
|
Definition
tunica intima (inner layer)
– endothelial lining with
basement membrane
– some connective tissue (CT)
• tunica media (middle)
– variable muscular elements –
regulate diameter
– variable elastin – “elastic
lamina”
• tunica adventitia or externa
(outer)
– variable connective tissue
– extensive blood and nerve
supply (VASOVASORUM) |
|
|
Term
| what are some similarities and differences between cardiac and skeletal muscle? |
|
Definition
Similar to skeletal
muscles
– sarcomeres
– actin/ myosin
• Differences from skeletal
muscle
– mononucleated
– branched
– connect through
intercalated disks
(gap junctions,
desmosomes) |
|
|
Term
| what are the intercalated disks? |
|
Definition
Interconnected by intercalated discs, form functional syncytia
• Within discs – two kinds of membrane junctions
– Desmosomes
– Gap junctions |
|
|
Term
| What are some differences between the t-tubules and SR of cardiace muscle vs skeletal muscles? |
|
Definition
T-tubules, larger than
in skeletal muscle, are
aligned with Z-disks
(one per sarcomere)
SR is juxtaposed with
T-tubules at very small
terminal bulbs, rather
than large cisternae
SR is thin and lacy, with
much smaller volume
than skeletal SR |
|
|
Term
| what are the two types of cardiac muscle cells? |
|
Definition
Contractile cells (99% cardiac cells)
• Do mechanical work of pumping
• Normally do not initiate own APs
– Autorhythmic cells
• Send electrical signals to the contractile cells
• Specialized for initiating and conducting action potentials
responsible for contraction of working cells
• Locations:
– Sinoatrial node (SA node)
– Atrioventricular node (AV node)
– Bundle of His (atrioventricular bundle)
– Purkinje fibers |
|
|
Term
|
Definition
| self firing. can be normal, or it can be pathological. |
|
|
Term
| what are the 4 parts that are the electrical conduction system of the heart? |
|
Definition
SA node
– right atrial wall near superior
vena cava
– Pacemaker of the heart
• AV node
– base right atrium
– only connection to ventricles
• Bundle of His (AV bundle)
– at AV node towards
interventricular septum
– Form R and L bundle
branches down septum,
• Purkinje fibers – extend
from Bundle of His through
ventricles |
|
|
Term
| how do the autorhythmic cells work? |
|
Definition
Pacemaker potential
– small Na+ leak (Lf) -"funny" channels
– open when Vm more negative than ~ -50 mV
– (plus some T- Ca 2+channels)
Threshold
– depolarization at ~ -40 mV
– L - Ca channels open,
• Repolarization
–Slow K+
channels open
–close Ca2+
channels |
|
|
Term
| How does the autorhythmic cells contract? |
|
Definition
when the cell is HYPERpolarized, the ifunny channels open and allow sodium and some (transient) calcium (channels) into the cell, driving membrane potential up.
When threshold is reached, long lasting calcium channels open causing the main depolarization.
at peak potential, slow K+ channels open, and close Ca+2 channels. |
|
|
Term
| how do the contractile cells work? |
|
Definition
No pacemaker potentials –
driven by pacemaker cells
• Threshold/depolarization classic fast Na+ channels
• Plateau phase – elevated L-type
Ca
2+
channels (dihydropyridines)
• Repolarization- Slow ("delayed
rectifier") K
+
channels open/ close
Ca
2+ channels; close to restart
cycle
instead of depolarizing quickly, long lasting calcium channels keep it high for a while. then slow delayed K+ channels open and Ca+2 channels close.
dihydropyridines are calcium channel blockers and reduce the amount of time the contraction lasts, so we can decrease the heart workload |
|
|
Term
| if you knock off the SA node, what happens? |
|
Definition
the other nodes take over
Normal frequency - SA node - 70 bpm
AV node - 50 bpm.
purkinje fibers - 20-30 bpm |
|
|
Term
| how does calcium signaling work in cardiac muscle? |
|
Definition
1. the action potential enters from an adjacent cell.
2. voltage gated Ca+2 channels open. calcium enters the cell (dihydrapyridine receptor)
3. calcium induces calcium release through ryanodine channels
4. local release causes ca+2 spark
5. summed calcium sparks create a Ca+2 signal.
6. Calcium ions bind to troponin to initiate contraction
7. relaxation occurs when calcium unbinds from troponin.
8. calcium is pumped back into the SR for storage
9. calcium is exchanged with Na+ (1 calcium out per 3 sodiums in)
10. Na+ gradient is maintained by the Na/K pumps. |
|
|
Term
| what things influence calcium entry into heart cells? |
|
Definition
| epinephrine drives calcium concentration up, Ach drives it down. |
|
|
Term
| how does epinephrine modulate cardiac excitation? |
|
Definition
| sympathetic - Depolarize Vm at baseline, increases “funny” current. |
|
|
Term
| epinephrine activates which receptors? |
|
Definition
| Beta 1. this increases cAMP. increase Ca+2 channel conductance |
|
|
Term
| Acetylcholine activates which receptors? |
|
Definition
| muscarinic receptors - decrease cAMP, which decreases Ca+2 entry. |
|
|
Term
| what are dihydropyradines? |
|
Definition
| L-type calcium channels respond to dihydropyridine drugs and block the activity of the channel. they reduce how much calcium comes in and how long it stays on, so it reduce the force of the heart contraction. |
|
|
Term
| how does acetylcholine modulate cardiac excitation? |
|
Definition
| parasympathetic – muscarinic receptors. Hyperpolarize Vm, decreases “funny" channels. |
|
|
Term
|
Definition
Record of overall spread of electrical activity through heart
– part of activity in body fluids by APs that reaches body surface
– not direct cardiac recording
• Overall spread throughout heart during depolarization
and repolarization/not single Aps
• Comparing V differences
on body surface
– not actual potential
– no potential recorded
with heart completely
depolarized/
repolarized |
|
|
Term
|
Definition
|
|
Term
|
Definition
| AV nodal delay (and full atrial contraction) |
|
|
Term
|
Definition
| ventricular depolarization (atria repolarizing simultaneously) |
|
|
Term
|
Definition
| time during which the ventricles are contracting and emptying. |
|
|
Term
|
Definition
| ventricular repolarization |
|
|
Term
| what is the TP internval? |
|
Definition
| time during which ventricles are relaxing and filling. |
|
|
Term
| what is a normal heart rate? tachycardia? bradycardia? |
|
Definition
normal = 70 bpm
tachycardia = >100 bpm
bradycardia = <60 bpm |
|
|
Term
|
Definition
diastole = relaxation low pressure
systole = contraction high pressure |
|
|
Term
| what are some arrhythmias? |
|
Definition
Atrial flutter (200-300 BPM) vs fibrillation (irregular)
– Ventricular fibrillation
– Premature Ventricular Contraction (PVC) (this is caused by ectopic or self initiated contractile cells) |
|
|
Term
| what are the 3 degrees of heart block? (dissociated atrial and ventricular) |
|
Definition
- 1st degree – PR fixed > 0.2 sec
•2nd degree (two types)
– PR gradually lengthened, then drop
QRS
– PR fixed, drop QRS randomly
•3rd degree block - PR and QRS
dissociated |
|
|
Term
| what are the mechanical evens of the cardiac cycle? |
|
Definition
1. Rest (atria/ventricles in diastole – filling with low pressures)
2. Atrial Systole – completes ventricular filling
3. Isovolumetric Ventricular Contraction
– Increased pressure in the ventriclescauses the AV valves to close…
why? (1st
heart sound)
– Atria go back to diastole
– No blood flow as semilunar valves are closed as well
4. Ventricular Ejection – interventricular > aortic pressure (semilumar
valves open)
5. Isovolumetric Ventricular Relaxation - interventricular < aortic
pressure (Semilunar values close – 2
nd heart sound) |
|
|
Term
| what are the cardiac phases? |
|
Definition
1. Rest (atria/ventricles
in diastole)
2. Atrial Systole
3. Isovolumetric
Ventricular
Contraction
4. Ventricular Ejection
5. Isovolumetric
Ventricular
Relaxation |
|
|
Term
| why do the AV valves close? |
|
Definition
| pressure in the ventricle is higher than the atria. |
|
|
Term
| in the isovolumetric contraction, why are the semilunar valves closed? |
|
Definition
| the pressure in the aorta/pulmonary trunk is higher than the pressure in the ventricles |
|
|
Term
|
Definition
= heart rate
(HR) x stroke volume (SV)
– SV ~ 70 ml
– HR ~ 70 beats/min
– Output about 5 L/min at rest
– Increase to 30-40 L/min during
high intensity exercise |
|
|
Term
| how is stroke volume determined? |
|
Definition
by extent of venous return
and by contractility/afterload |
|
|
Term
|
Definition
end-diastolic volume (EDV)
– Increases “pre-load”
• Amount of stretch within myocardium (‘load’ prior to contraction)
• Length-tension patterns (Frank-Starling Law)
– Determinants
• Skeletal muscle pump
• Respiratory pump
• Cardiac “Suction” |
|
|
Term
|
Definition
contributes to ESV
– Stronger contraction =
larger stroke volume
– “inotropic agents”
(epinephrine/NE; Ach
is opposite)
– Increased Ca
2+
entry/modulation –
more force per unit
muscle/length |
|
|
Term
| how does epinephrine increase contractility? |
|
Definition
it binds to beta 1 receptors, activates cAMP second messenger system, which opens voltage gated calcium channels.
also it phosphorylates phospholamban, which increases activity of calcium atpase on the SR, increases calcium stores in the SR, which leads to a more forceful contraction, but ALSO calcium is removed from the cytosol faster, shortening the ca-troponin binding time, which leads to a shorter duraction of contraction |
|
|
Term
|
Definition
contributes to ESV
– aortic pressure to overcome to
open semilunar valves
– Higher afterload - reduces
ejection fraction (SV/EDV) ~
normal=52%
– indirect relationship- Higher
aortic pressure = lower stroke
volume
– Causes?
• Elevated blood pressure
• Loss of compliance in aorta
(loss of elasticity) |
|
|
Term
| what is ejection fraction? |
|
Definition
ejection fraction (SV/EDV) ~
normal=52% |
|
|
Term
| when you damage the vessels because of high pressure repeatedly, what happens? |
|
Definition
| you can't lay down the elastin that you want. you lay down collagen, which is much stiffer. |
|
|
Term
| what are pressure volume curves? |
|
Definition
Pressure/Volume relation often plotted to indicate demands on cardiac tissue
– Start at (a) diastole, (b)-(c) systole, (d)-(a) diastole
– Curve runs counter-clockwise. |
|
|
Term
|
Definition
end diastiolic pressure volume relationship, slope of the A line
end systolic pressure volume relationship. slope at point 3. |
|
|
Term
LEFT VENTRICULAR
PRESSURE/VOLUME CURVE |
|
Definition
A. mitral valve opens
– Heart relaxation
– vent P
atrial P)
– Rapid increase in pressure
(no change in volume no
valves open)
D. aortic valve opens
– Vent P > aortic P
– Blood starts to be ejected
E. systole (cont)
– Decreased vent volume
with blood ejection
– Maintaining high pressures
F. start of diastole
– Aortic valve closes (vent P
< aortic P)
– Rapid drop in pressure (no
change in volume – no
valves open) |
|
|
Term
| what are the effects of preload on the ventricular P/V loop? |
|
Definition
| it would increase EDV, or shift the EDV point to the right (increasing stroke volume) |
|
|
Term
| what would an increase in contractility do to the ventricular P/V loop |
|
Definition
| increase in ESV, and ESPVR, higher stroke volume. shifts the top left corner higher (and higher right top corner). increase slope of ESVPR line |
|
|
Term
| what would an increase in afterload look like on a PV loop? |
|
Definition
| increase in the top right corner, but shifting the ESV a bit to the right, so you stop short essentially. no change in slope of ESPVR line. |
|
|
Term
| What is coronary arterial disease? |
|
Definition
Primary cause of mortality in US
– Can cause myocardial ischemia or
infarction (3 mechanisms)
• Vascular spasm of coronary arteries
• Formation of atherosclerotic plaques
• Thromboembolism
– Angina Pectoris (chest pain, can be cause by ischemia)
• Controlled w/ exertion (can titrate exertion)
• Uncontrolled – vasospasm (very bad) |
|
|
Term
| what are some possible outcomes of post-myocardial infarction? |
|
Definition
Immediate death –
– heart ineffective in pump function
– fatal ventricular fibrillation 2⁰
damage conducting tissues
• Delayed complications/death –
– Fatal rupture of dead/degenerating
cardiac wall
– Progressive heart failure
• Full recovery
– Replacement of damaged wall with
scar
– Enlargement, compensation of
remaining contractile tissue
• Recovery with impaired function
– Permanent functional defects
– bradycardia, conduction blocks |
|
|
Term
| how is structure related to function for the aorta, arteries, arterioles, capillaries, venules, and veins? |
|
Definition
Structure allows function
– Aorta – absorb pulse pressure (SBP - DBP)
– Large arteries conduct/distribute blood to specific regions
– Arterioles – regulate flow and
mean arterial pressure (MAP)
– Capillaries – exchange
– Venules – collect/direct blood
to veins
– Veins – return blood to heart/reservoir |
|
|
Term
| what is mean arterial pressure? |
|
Definition
Mean Arterial Pressure (MAP)
• MAP = DP + 1/3 Pulse Pressure
OR it can be 1/3 SBP + 2/3 DBP
• Evaluates general health of CV system |
|
|
Term
|
Definition
| systolic blood pressure - diastolic blood pressure. |
|
|
Term
| how is BP measured, and what are korotkoff sounds? |
|
Definition
Measured indirectly using
sphygmomanometer
• Korotkoff sounds
– Sounds heard when determining blood
pressure
– Sounds are distinct from heart sounds
associated with valve closure |
|
|
Term
| what sounds to you hear when taking a BP? |
|
Definition
1. Cuff pressure > SBP -No sound.
2. The first sound is heard at peak SBP.
3. Sounds are heard while cuff pressure < SBP but > DBP
4. Sound disappears when cuff pressure < DBP |
|
|
Term
we defined mean arterial pressure earlier as DP + 1/3 Pulse Pressure
OR it can be 1/3 SBP + 2/3 DBP. Why is MAP so important for fluid flow in your body? |
|
Definition
| mean hydrostatic pressure gradient driving fluid flow (depends on blood volume/vessel compliance) |
|
|
Term
|
Definition
– ease of flow through vessels, total peripheral
resistance (TPR) proportional to MAP and CO
– With increased resistance but similar CO, what happens to
MAP? - increased Mean arterial pressure
– With anaphalaxis, what happens to resistance, MAP, CO? - huge vasodilation, pressure goes way down with resistance, cardiac output tries to keep up |
|
|
Term
| what is "ohm's law for fluids"? |
|
Definition
| mean arterial pressure (potential difference) = cardiac output (flow or current) x total peripheral resistance (R). |
|
|
Term
| how is blood flow to reconditioning organs? |
|
Definition
Reconditioning organs receive more
blood than metabolic needs
– Digestive organs, kidneys, skin
– Adjust extra blood for homeostasis
• Blood flow to other organs can be
adjusted according to metabolic needs
• Brain can least tolerate disrupted
supply |
|
|
Term
| what is important about arterioles? |
|
Definition
Major resistance vessels
– Radius adjusted independently to
distribute CO
– Help regulate arterial blood pressure
• Histology/function
– Larger arterioles – reduced elastic fibers
from arteries, increased muscle fibers
– Smaller arterioles - relatively greater
smooth muscle
• Adjusting arteriolar resistance
– Vasoconstriction - narrowing a vessel
– Vasodilation – increase vessel radius
– Alter smooth muscle contractions |
|
|
Term
| what are the characteristics of smooth muscle in arterioles? |
|
Definition
Characteristics
– Walls of hollow organs/tubes
– No striations (no sarcomeres/
myofibrils)
– Spindle-shaped cells, single
nucleus
• Cells usually arranged in
sheets within muscle
• Have dense bodies containing
same protein found in Z lines
• Filaments/structures
– myosin (thick) - Longer than those
in skeletal muscle
– actin (thin) - Contain tropomyosin,
no troponin
– Intermediate - part of
cytoskeleton, not directly related to
contraction |
|
|
Term
| how are smooth muscles activated? |
|
Definition
Ca2+ dependent 2nd messenger
– Increased Ca 2+ entry from ECF
– Result in phosphorylation of
myosin thick filament
– Actin-myosin interaction |
|
|
Term
| what is a multi-unit vs single unit smooth muscle? |
|
Definition
Multi-unit
– Neurogenic
– Discrete units that function independently of one another
– Units must be separately stimulated by nerves to contract
– Locations (large blood vessels, large airways, vision (iris/lens),
hair follicles
• Single-unit
– Self-excitable (does not always require PNS for contraction)
– Visceral smooth muscle
– Fibers become excited and contract as single unit
– gap junctions/desmosomes interconnecting - “functional
syncytium”
– Slow/energy-efficient contractions - distensible, hollow organs |
|
|
Term
| what is opposition to blood flow in arterioles? |
|
Definition
Resistance (R) directly
proportional to:
• vessel length (L),
• blood viscosity(η),
• inversely proportional of
radius (to the 4
th
power)
R L η/r
4
– L and ηconstant, so R 1/r
4 |
|
|
Term
| what controls vessel diameter? |
|
Definition
Vessel diameter controls
are local and systemic
– Enables tissues to control
their own blood flow
– Local controlling
mechanisms include intrinsic
and extrinsic |
|
|
Term
| what are some of the intrinsic responses that change vessel diameter? |
|
Definition
Myogenic responses - stretch with
increased pressure (mechanicalgated Ca
2+
channels)
– Paracrine vasoconstrictors
• Serotonin – activated platelets
• Endothelin – by endothelium
– Paracrine vasodilators
• NO – by endothelium
• Bradykinin/histamine/prostaglandins
(inflamm)
• Adenosine – hypoxic cells
• O2
, CO2
, K+
, H+
, temp |
|
|
Term
| what are some extrinsic responses that change vessel diameter? |
|
Definition
Vasocontrictors
• NE – sympathetic postganglionic
• Vasopressin (ADH) – post pituitary
(CNS release with low BP)
• Angiotensin II – part of reninantiogensin pathway
– Renin from kidneys
– Angiotensinogen to Angiotensin I
– To Angiotensin II at lungs (ACE)
– Vasodilators
2
Epi (adrenal medulla)
• Ach – parasymp postganglionic
• ANP (atrial natriuretic peptide) –
atrial myocaridum /brain
• VIPs (vasoactive intestinal
peptides) – from neurons |
|
|
Term
|
Definition
| lowers blood pressure by stopping conversion of angiostensin 1 to angiotensin 2 in the lungs. |
|
|
Term
| where would you vasodilate with epinephrine? |
|
Definition
| coronary arteries, possible skeletal muscle |
|
|
Term
|
Definition
Hyperemia is locally mediated increases in blood flow (active or reactive)
active = an increase in tissue metabolism releases metabolic vasodilators into ECF. arterioles dilate, blood flow increase, nutrients are supplied to the tissues
reactive = decreased blood flow due to occlusion releases metabolic vasodilators into the ECF, arterioles dilate, BUT occlusion prevents the blood flow |
|
|
Term
Vasoconstriction/dilation
depending on demands. what would be the demands at rest and during exercise? |
|
Definition
–Rest
• Vasodilation – Ach release
(parasymp) at GI/splanchnic
• Vasoconstriction (no NE release,
locally mediated - not much constriction. enough to not die)
– Exercise
• Vasodilation – dominated by
metabolic factors at local active
muscle (active hyperemia)
• Vasoconstriction – NE mediated - definitely constricting in GI, other areas are controversial |
|
|
Term
| what is a normal sinus rhythm? |
|
Definition
| its means the p wave is both in the same direction and happens before the QRS wave |
|
|
Term
| is the pressure in the left ventricle higher when the aortic valve opens, or when it closes? |
|
Definition
| the point when the aortic valve closes is always at a higher pressure than when it opens. |
|
|
Term
| what does the cardiovascular control center do? |
|
Definition
| Receives inputs from carotid and aortic baroreceptors. Then it sends signals to the autonomic nervous system, both sympathetic and parasympathetic. |
|
|
Term
| what types of receptors, and what tissue types, does sympathetic activity elicit? |
|
Definition
| alpha receptors on arteriolar smooth muscle. beta 1 receptors on ventricular myocardium and SA node. |
|
|
Term
| how does flow, velocity, pressure, and resistance change throughout the cardiovascular system? |
|
Definition
Flow constant, decrease in
velocity with increased crosssectional area
• Pressure drop with blood
movement/friction along vessel
length. velocity decreases in capillaries with increased cross sectional area. |
|
|
Term
| why would we want a slow velocity of blood in capillaries? |
|
Definition
| more time to exchange gases, metabolic products, etc. |
|
|
Term
| what are the two ways things passively exchange in capillaries? |
|
Definition
|
|
Term
| what are some factors that affect diffusion rate in capillaries? |
|
Definition
area, permeability, concentration gradient, diffusion
distance |
|
|
Term
| what are water filled gaps in capillaries called that are specialized for water transport? |
|
Definition
|
|
Term
| how do lipids get through capillaries? |
|
Definition
| they diffuse right through |
|
|
Term
|
Definition
Hydrostatic Pressure (P) and Osmotic (oncotic)Pressure (pi symbol).
Driving forces into blood
– hydrostatic interstitial pressure (PIF)
– osmotic blood pressure (piC)
Driving forces out of blood
– hydrostatic blood pressure (PC)
– osmotic interstitial pressure (piIF) |
|
|
Term
| at the beginning of the capillary you have net outflow. why? |
|
Definition
| the hydrostatic blood pressure in the capillary is higher than the oncotic pressure in the capillary. |
|
|
Term
| at the end of the capillary you have a net inflow. why? |
|
Definition
| the hydrostatic blood pressure in the capillary is less than the oncotic pressure. |
|
|
Term
| in the capillaries, a little bit more fluid goes out than comes back in. where does the extra fluid go? |
|
Definition
|
|
Term
| what is the structure and function of the lymphatic system? |
|
Definition
Function
– Return of excess filtered fluid and protein
– Defense – nodes with lymphocyte aggregates
– Transport of absorbed fat
• Structures
– Blind-ending capillaries (overlapping endothelial
cells) throughout IF
– Lymphatic vessels - drainage
– Drainage between |
|
|
Term
| what happens when you have liver damage? |
|
Definition
| less albumin, so less oncotic pressure, so more outflow from capillaries, less reabsorption, so you have widespread systemic edema. |
|
|
Term
| if you cant get blood into the liver, it backs up into the GI system. what happens to those capillaries? |
|
Definition
| the capillaries have a much higher hydrostatic pressure, so more filtration, less reabsorption, and you have a localized edema in the GI, called ascites. |
|
|
Term
| what is the general structure and function of the veins? |
|
Definition
Structures
– Capillaries to venules, to small/large veins
– Mostly collagen/little elastin (“valves” in larger veins)
– Variable muscular tissues
– Leaky in venules (inflammatory cells)
• Function: return blood to heart
– Large radius = little resistance
– “reservoir” – capacitance vessels |
|
|
Term
| normally, is most of your blood is in your veins or arteries?. |
|
Definition
|
|
Term
| what are some factors that affect or enhance venous return. |
|
Definition
–Gravity
– Initial blood pressure, cardiac “suction”
– Venous vasoconstriction
– Skeletal/respiratory muscle activity
(venous valves) |
|
|
Term
| how does the sympathetic nervous system affect venous return? |
|
Definition
| it causes venoconstriction, increasing venous pressure, increasing venous return. |
|
|
Term
| what are the effects of increased venous return again? |
|
Definition
| increase EDV, increase stroke volume, increase cardiac output. |
|
|
Term
| what is the primary determinants of mean arterial pressure? |
|
Definition
| mean arterial pressure = cardiac output X total peripheral resistance. |
|
|
Term
| why is blood pressure so heavily monitored and regulated by your body? |
|
Definition
it makes sure there is adequate driving pressure into the brain and organs, and it prevents extra work.
Short-term control adjustments (secs)
– Adjustments made by alterations in cardiac output and total
peripheral resistance
– Mediated by ANS influences on heart/vasculature
• Long-term control adjustments (minutes/days)
– adjusting total blood volume
– restoring normal salt and water balance via thirst, renal system
(aldosterone/ADH) |
|
|
Term
| what are some additional factors influencing CV function? |
|
Definition
Left atrial receptors and hypothalamic osmoreceptors - longterm regulation of BP via plasma volume (ANP) (vasopressin and antidiuretic hormone)
• Chemoreceptors (carotid/aortic bodies) are sensitive to low O
2
or high acid levels in blood –increase respiratory activity
• Associated with certain behaviors and emotions mediated
through cerebral-hypothalamic pathway
• Exercise modifies cardiac responses
• Hypothalamus controls skin arterioles for temperature
regulation |
|
|
Term
| what are the differences between primary hypertension and secondary hypertension? |
|
Definition
Primary - Catch-all for increased BP by variety of unknown
causes (vs single disease entity)
– Defects in renal Na regulation/excessive Na intake
– Diets low in K
+
and Ca
2+
– Plasma membrane abnormalities (defective Na
+-K
+
pumps)
– Gene variation for angiotensinogen
– Abnormalities in NO, endothelin, or other local-acting
chemicals
– Excess vasopressin
• Secondary hypertension (10% cases) – renal, endocrine, neurogenic |
|
|
Term
| what are some possible complications from hypertension? |
|
Definition
Cardiac failure
• Atherosclerosis (stroke, heart attack)
• Spontaneous hemorrhage/aneurysm
• Renal failure
• Retinal damage |
|
|
Term
| renin converts angitoensin I to angiotensin II....???? google this. |
|
Definition
|
|
Term
|
Definition
- adaptive mechanisms to compensate for altered physiology
• deleterious structural changes with increased compensation
• Increased O
2demands of heart vs decreased blood supply
• Mismatch leads to ischemia (may lead to angina) |
|
|
Term
| what is congestive heart failure? |
|
Definition
heart cannot pump or fill adequately
• division of circulation that requires most work usually
the most affected
• where does blood back up? the lungs
• what could we expect from such a back-up? pulmonary edema from increased filtration in the lungs, less reabsorption, trouble breathing. |
|
|
Term
| what are some potential causes of cardiac failure? |
|
Definition
Hypertension –
– Adaptive response to increased stretch (filling) and increased NE
release/effects
– Both have immediate and long-lasting (trophic) effects on
cardiac function
• Myocardial infarction:
– Impaired cardiac muscle function – decrease “pump” capacity (systolic failure)
– Damaged, non-regenerative muscle – scar formation leads to loss of tissue distensibility (diastolic failure - pericarditis)
• Additional causes:
– Altered blood flow regulation (regurgitation)
• Valve incompetence
• Oxygenated blood flow to deoxygenated blood sources
– Valve stenosis
septal defects, valvular disease |
|
|
Term
| what is dilated cardiomyopathy? |
|
Definition
| you stretch the heart past the optimum area on the length tension curve. stretched heart without compensating muscular hypertrophy. |
|
|
Term
|
Definition
form of arteriosclerosis (‘hardening’)
– intimal wall thickening
– collagen deposition, loss of elastic tissue (think tissue
healing and scar formation) |
|
|
Term
| what are the stages of atheroma? |
|
Definition
1st stage - sub-endothelial accumulation of cholesterol (aka
fatty streak)
– 2nd stage - smooth muscle migration, division, enlargement
– 3rd stage - plaque formation, calcification
also monocytes become macrophages which become foam cells which are bad. they form a necrotic center which is covered by a fibrous cap. |
|
|
Term
| what are some factors causing thrombosis? |
|
Definition
Virchow’s triad
• Abnormality of vessel wall
(endothelium)
• Abnormality of blood flow
• Alterations in blood contents |
|
|
Term
| with atherosclerosis how is the thrombus formed? |
|
Definition
formation of thrombus
– roughened surface, damaged endothelium,
stagnant blood
– breaking off of thrombus? thats an embolus . will occlude blood flow downstream
– stroke, heart attack, arterial insufficiency
– if have one disease, obvious predisposition for
other
with arterial damage – weakening can lead to
aneurysm
– out-pouching, held together by elastic lamina,
adventitia
– rupture – potential for massive blood loss
– other causes?? Genetic? Marfans. Environmental? COCAINE |
|
|
Term
| what is hypotension, and what are some of the types? |
|
Definition
Low blood pressure (BP < 100/60 mm Hg)
– There is too little blood to fill the vessels
– Heart is too weak to drive the blood
• Orthostatic (postural) hypotension
– Transient (typically)
– insufficient compensatory responses to gravitational
shifts
• Circulatory shock – when BP falls
– BP falls, inadequate flow to tissues
– Hypovolemic, cardiogenic, vasogenic, neurogenic |
|
|
Term
| what causes hypovolemic shock? |
|
Definition
| severe hemorrhage, excessive vomiting, diarrhea, urinary losses |
|
|
Term
| what causes cardiogenic shock? |
|
Definition
|
|
Term
| what causes neurogenic shock? |
|
Definition
| septic shock or anaphylactic shock causing massive vasodilation |
|
|
Term
| what causes vasogenic shock? |
|
Definition
| decreased sympathetic nerve activity,vasodilation |
|
|
Term
| what is venous insufficiency, and what are some types? |
|
Definition
loss of valve integrity
• external dilations/ contortions of
superficial veins
• varicosites
– chronic – genetic component,
manifest in legs
– esophagus, anal plexus –
secondary to portal hypertension
– hemorrhoids – pregnancy,
constipation |
|
|
Term
| what are some differences in arterial vs venous insufficiency/ulceration? |
|
Definition
Sustained venous hypertension -venous ulceration
– 10% population with valvular
incompetence, 0.2% with ulceration
– Clinical features
• Pitting edema - preceded
ulceration, greater later in day
• Hemosiderin pigmentation
• Lipodermatosclerosis – indurate,
fibrotic subcutaneous tissue
• Atrophic, sweat gland/hair follicle
loss
VENOUS insufficiency/ulceration
-Hemodeserin (brown discoloration)
-lipodermatosclerosis
Arterial insufficiency/ulceration
-Punch-out ulceration
-Champagne bottle deformity (can occur in either)
• Atherosclerosis of peripheral
vasculature – arterial ulceration
– Other causes: diabetes, thromboangitis,
vasculitis
– Resultant tissue hypoxia and damage |
|
|
Term
| what is systemic and localized edema? |
|
Definition
Regulation of fluid via oncotic vs. hydrostatic
pressures
– Hydrostatic
• Increased BP
• Fluid accumulation/backup
– “Pump” failure
– Drainage failure
– Oncotic
• altered plasma proteins
• albumin production |
|
|
Term
| what are some clinical pharmacology implications for hypertension? |
|
Definition
Diuretics – increase Na excretion (thiazides)
• Sympatholytic drugs
– blockers – vasodilation
– blockers – decrease HR and contractility
• Vasodilator drugs (hydralazine, minoxidil)
• Calcium antagonist drugs
– Verapamil and diltiazem act on heart and vessels to lower BP
– Nifedipine - lower BP only by vasodilation
– also used to treat angina pectoris and cardiac arrhythmias
• ACE inhibitors
– inhibit formation of angiotensin II – less vasoconstriction
– decrease aldosterone release - decreased Na, H20 retention |
|
|
Term
| what are some clinical pharmacology implications for angina pectoris or Coronary artery disease? |
|
Definition
Nitrites and nitrates (amyl nitrate, nitroglycerin)
– NO - potent vasodilator of all blood vessels
– Raipdly decreases cardiac work, oxygen consumption
– Decrease BP may cause reflex tachycardia, dizziness,
hypotention
• blockers
– decreases cardiac work, oxygen demands
– used prophylactically to prevent angina,
– Blunted HR responses to exercsie
• Ca channel blockers – act on myocardium or vessels |
|
|
Term
| what are some clinical pharmacology implications for congestive heart failure? |
|
Definition
Digoxin and digitoxin
– Main effect: increase myocardial contractile force
• inhibit Na/K ATP pump, more Na inside myocardial cells
• Increased intracellular Na stimulates Na/Ca exchange,
• more Ca entry increases contractility
– Cardiac glycosides also decrease heart rate and
atrioventricular conduction (vagal stimulation)
• Also utilize diuretics, vasodilators to decrease work of
heart |
|
|
