Physiology Flashcards
(220 cards)
1
Q
What % of the body mass is water?
A
60
2
Q
Intracellular fluid makes up _____ of total body water
A
2/3
3
Q
Extracellular fluids makes up ____ of total body water
A
1/3
4
Q
What is the ECF composed of?
A
3/4 is ISF
1/4 is PV
5
Q
What does the vascular compartment of total body water contain? Where is it?
A
Blood volume, which is plasma and the cellular elements of blood (especially RBC)
ECF
6
Q
What separates ISF from vascular volume?
A
capillary membranes
7
Q
What is the difference between osmolarity and osmolality?
A
Osmolarity = mOsm/L Osmolality = mOsm/kg of water
8
Q
What is the term for a solute that does not easily cross the membrane?
A
“Effective” osmole
9
Q
Is sodium an example of an osmole? Why or why not?
A
Yes for the ECF as Na can not cross the cell membrane easily but can cross the capillary membrane easily
10
Q
What is a basic metabolic profile?
A
The common labs provided from a basic blood draw
11
Q
What is the osmolar gap?
A
It is the difference between the measured osmolality and the estimated osmolality
12
Q
How do we calculate the osmolar gap?
A
ECF estimated osmolality: 2(Na) mEq/L + glucose mg%/18 + urea mg%/2.8
13
Q
What is a normal osmolar gap?
A
<15
14
Q
Examples of loss of isotonic fluid? (3)
A
Hemorrhage, diarrhoea, vomiting
15
Q
What happens to the body compartments and osmolarity if you lose isotonic fluid?
A
Decrease in ECF volume
No change in body osmolarity or ICF volume
16
Q
How does the D-Y diagram change if you lose isotonic fluid?
A
the vertical dotted line on the right side moves inward
________ _____
| | –> | |
————— ———-
17
Q
D-Y diagram features
A
Vertical: concentration of solute
Horizontal: left = ICF volume, right = ECF volume
18
Q
What happens to the body compartments and osmolarity if you lose hypotonic fluid?
A
Both ICF and ECF decrease, increase in body osmolarity
19
Q
Examples of loss of hypotonic fluid?
A
Dehydration, DI, alcoholism
20
Q
Gain of isotonic fluid example?
A
Saline
21
Q
What happens to the body compartments and osmolarity if you gain isotonic fluid?
A
Increased ECF volume, no change to the ICF volume or body osmolarity
22
Q
Gain of hypotonic fluid example?
A
Hypotonic saline, water intoxication
23
Q
What happens to the body compartments and osmolarity if you gain hypotonic fluid?
A
Increased ECF volume, decreased body osmolarity, increased ICF volume
24
Q
What happens to the body compartments and osmolarity if you gain hypertonic fluid?
A
Increased ECF volume, increased body osmolarity, decreased ICF volume
25
What are the 2 primary factors stimulating aldosterone release?
K+
| Angiotensin II
26
What are the 2 primary regulators of ADH release?
```
Plasma osmolarity (direct)
Blood pressure/volume (indirect)
```
27
2 ADH receptors and function?
```
V1 = vasoconstriction
V2 = water reabsorption
```
28
Is renin a hormone?
No, renin is an enzyme
29
What does renin do?
Renin converts angiotensinogen to angiotensin I, which in turn is converted to Any II by ACE
30
What are the 3 primary regulators of renin release?
GFR (inversely related)
Sympathetic stimulation to the kidney (via B1)
Na delivery to macula dense (inversely related)
31
In terms of pressures, what does P and pi stand for?
```
P = hydrostatic
pi = osmotic
```
32
Filtration vs absorption
Filtration is the movement of fluid from the plasma into the interstitial
Absorption is the movement of fluid from the interstitial into the plasma (capillary)
33
Absorption pressures
piCapillary
| PInterstitial
34
Filtration pressures
piInterstitial
| Pcapillary
35
What is Pc directly related to?
BP, venous flow, BV
36
What protein is the biggest contributor to the piC?
Albumin!
37
Starling equation =
Qf = k [(Pc + piIF) - (PIF + piC)]
38
Positive Qf =
net filtration
39
Negative Qf =
net absorption
40
How to lymphatics contribute to the interstitial fluid volume and protein content?
Directly proportional to interstitial fluid pressure, thus a rise in this pressure promotes fluid movement out of the interstitium via lymphatics
41
Which veins do the lymphatics drain into?
Subclavian
42
Is pitting or non-pitting oedema more common?
Pitting
43
What is pitting oedema?
Pressing the affected area results in visual indentation of the skin
Responds well to diuretic therapy
44
What is non-pitting oedema?
Does not indent when pressing area, this occurs when interstitial oncotic forces are elevated, it does not respond well to diuretic therapy
45
What causes peripheral oedema? (all of the forces and the causes for change)
Increased Pc = marked increase in blood flow, increased venous pressure (i.e. heart failure), elevated blood volume
Increased piIF = thyroid dysfunction (elevated mucopolysaccharides in interstitial) = non-pitting
Decreased piC = liver failure and nephrotic syndrome
Increased k = TNF-a, bradykinin, histamine, cytokines
Lymphatic obstruction: elephantiasis, strep, trauma, surgery, tumour, non pitting because increased piIF
46
What is "k"?
Capillary permeability
47
What can pulmonary oedema lead to?
hypoxemia and hypercapnia
48
2 causes of pulmonary oedema (forces)
1. Cardiogenic - elevated Pc (most common)
| 2. Non-cardiogenic - decreased permeability (ARDS)
49
What causes cardiogenic pulmonary oedema?
Increased left arterial pressure increases venous pressure = increased capillary pressure
Initially increased lymph flow reduces proteins and is protective
Elevated pulmonary wedge pressure
50
First sign of cardiogenic pulmonary oedema and treatment?
Orthopnea (dyspnea laying down)
| Diuretics
51
How does non-cardiogenic pulmonary oedema happen?
Direct injury of alveolar epithelium or after a primary injury to the capillary endothelium
Fluid accumulation as a result of the loss of epithelial integrity
Presence of protein-containing fluid in alveoli inactivates surfactant causing reduced lung compliance
Pulmonary wedge pressure is normal or low
52
Causes of non-cardiogenic pulmonary oedema? signs?
sepsis, bacterial pneumonia, trauma, ARDS
| Rapid onset dyspnea, hypoxemia, and diffuse pulmonary infiltrates = respiratory failure
53
How do you calculate volume of the compartment?
amount of tracer/concentration of tracer in the compartment to be measured
54
Volume =
D/C
55
Tracer for.. Plasma, ECF, TBW
Albumin, inulin/sucrose/sodium, tritiated water/urea
56
Fractional concentration of RBC is also known as
Haematocrit
57
Blood volume =
Plasma volume/1-haematocrit
58
What % of body is blood volume?
Approx. 7%
59
What is membrane potential?
Separation of charge across membrane at rest
60
What is electrochemical gradient?
combination of 2 forces, chemical based on chemical concentration, electrical based on charge
61
What is conductance?
flow of an ion across membarne
62
What is an ungated ion channel?
always open, direction of ion move depends on EC forces
| resting membrane potential!
63
What is a voltage gated channel?
open/closed determined by membrane potential
64
What is a ligand gated channel?
channel has a receptor
| state of channel influenced by ligand to the receptor
65
What receptor is an exception to the 3 classes?
NMDA is both voltage and ligand
66
How is NMDA both ligand and voltage gated?
NMDA blocked by Mg2+ if Em is more negative than -70 (voltage)
NMDA ligands are glutamate and aspartate
67
What are NMDA receptors used for?
memory and pain transmission
68
Equilibrium is calculated via the _____ equation
Nerst
69
Depolarization less ____ hyper polarization more _______
negative
70
Hyperkalaemia ____ the cell
depolarizes
71
Hypokalaemia _____ the cell
hyper polarizes
72
What happens when the cell depolarizes?
nerves become excited
73
What happens when the cell hyper polarizes?
nerves decrease excitability
74
Na K relationship
2K in 3 Na out
75
3 states of a voltage gated Na+ channel
closed (rest), opened (activated), inactivated
76
closed state of voltage gated Na+ channel
activation gate closed (extracellular) and inactivation gate open (cytosol)
77
open state of Na+ channel
depolarization causes both channels to open
78
inactivated Na+ channel
activation gate open inactivation gate closed
79
What blocks fast Na+ channels?
extracellular Ca2+
80
what is the primary mechanism for depolarization?
K+ channels
81
explain what happens during an action potential
1. meets threshold
2. Na+ channels open = depolarization
3. AP becomes more positive and fast Na+ begin to inactivate
4. voltage gated K+ channels open in response to the depolarization, but kinetics are slower so more inward Na+ initially
5. K+ channels cause depolarization
6. K+ channels begin to close, and K+ slowly returns to its original level, because of slow kinetics, hyper polarization occurs
82
absolute vs relative refractory period
absolute: no matter how strong a stimulus, it cannot induce a second action potential
relative: greater than threshold stimulus is required to induce a second action potential
83
what influences conduction velocity in nerves? (2)
cell diameter (greater = greater), surface area (greater = less resistance), myelination (more myelin = more resistance across membrane, reducing current leak through the membrane, myelination is interrupted at nodes of Ranvier where Na+ channels cluster = bounces because faster = saltatory conduction)
84
NMJ events (6)
1. AP depolarizes presynaptic membrane
2. Ca2+ channels open, Ca2+ into presynaptic
3. Ca2+ in cell causes ACh to be released
4. ACh binds to nicotinic receptor = depolarization (ligand receptor)
5. open Na2+ channels = AP in sarcolemma
6. ACh terminated by AChE, choline taken back into pre
85
where does the NMJ synapse happen?
between axons of an alpha motor neurone and a skeletal muscle fibre
86
synaptic potentials are produced by
ligand gated ion channels
87
Does Ca2+ depolarize or depolarize the cell?
Depolarizes!
88
What is the primary mechanism for repolarization?
Voltage-Gated K+ channels
89
Where is the origin for the action potential of the axon? What is special about it?
Axon hillock - high density of fast Na+ channels
90
What is excitatory post synaptic potential?
Is excitatory if it increases the excitability of the postsynaptic neutron (more likely to fire an action potential) it is primarily the result of increased Na+g. It is similar to the EPP found at the neuromuscular junction
91
Which receptors produce EPSP?
nicotinic *endogenous ligand is ACh and includes Nm and Nn
non-NMDA *endogenous ligands are glutamate and aspartate
NMDA * endogenous ligands are the excitatory amino acids and it is a non-selective cation channel
92
What is inhibitory postsynaptic potential?
Inhibitory if it decreases the excitability of postsynaptic neutron, it is less likely to fire an action potential, primarily be result of increased Cl-
93
IPSP receptors
GABA
| glycine
94
3 section of PNS
Motor (alpha motor neurons)
Parasympathetic
Sympathetic
95
Alpha motor neurons bind to _____ and are ______ _______ neurons
Nm
| large, well-myelinated
96
Preganglionic parasympathetic neurons release _______ which binds to ______
ACh
| Nn receptor
97
Postganglionic parasympathetic fibres release ____ which binds to _____
ACh
| muscarinic (G protein coupled)
98
Preganglionic sympathetic neurons release______ which binds to _____
ACh, Nn
99
Postganglionic sympathetic neurons mostly release ______ which binds to ______
NE
| alpha and beta (1+3) receptors (G protein coupled)
100
Parasympathetic pre is short/long and post is short/long
long, short
101
Sympathetic pre is short/long and post is short/long
short, long
102
What is myasthenia graves?
autoimmune condition in which antibodies are created that block the Nm receptor
103
What is Lambert-eaton syndrome?
autoimmune condition in which antibodies are created that block the presynaptic voltage-gated Ca2+ channels
104
What cells in the heart are specialized for automaticity?
SA node cells
105
Who becomes the pacemaker if SA is damaged?
AV
106
Besides the SA and AV nodes, which ther part of the heart exhibits spontaneous depolarizations?
Purkinje cells
107
AV node cells are specialized for _____ conduction
slow
108
Purkinje cells are specialized for ______ conduction
fast
109
Why is the resting membrane potential close to K+? why?
potassium conductance is high in resting ventricular or atrial myocytes resulting from 2 channels
110
2 K+ channels
undated potassium channels - always open (potential -95)
| inward K+ rectifying channels -voltage gated that are open at rest, depolarization closes
111
Phase 0 of action potential in a myocyte, what happens and what part of the ECG?
conduction velocity is directly related to rate of change in potential, stimulation of B1 increases the slops
QRS
112
Plateau phase what happens and what part of the ECG?
depolarization opens voltage gated Ca2+ channels (L-type) and voltage gated K+ channels
ST segment
113
What part of the action potential prevents tetany in cardiac muscle?
plateau phase
114
Phase 3 of action potential in myocyte, what happens and what part of the ECG?
repolarization phase, T wave
115
In nodal cells, what happens in phase 4?
resting membrane potential
inward Ca2+ current (T-channels - more negative potential than L-type)
inward Na+ channel (HCN channel or funny current)
outward K+ current
116
Pacemaker potential aka
spontaneous depolarization potential
117
NE chornotropy and dromotropy
SA node: increased HR
| AV node: increased conduction velocity through AV node
118
NE in nodal cells does what?
NE from post-ganglionic sympathetic nerve terminals and circulating epinephrine, B1 receptors -> opens HCN and Ca2+ channels
increases slope of pacemaker potential
119
ACh in nodal cells does what?
from post-ganglionic fibres
M2 receptor opens K+ channels and inhibits cAMP
hyperpolarizses , reduces slope
120
ACh chronotropy and dromotropy
SA: decreased HR
| AV node: decreased conduction velocity through AV node
121
J wave on ECG
end point of the S wave, represents isoelectric point
122
y axis ECG units
mV
123
x axis ECG units
0.2 seconds
124
What is the mean electrical axis (MEA)?
net direction of current flow during ventricular depolarization
125
What is normal axis degrees?
-30 to +110 degrees
126
Which 2 leads do we use to determine MEA?
aVF and I
127
+aVF and I
normal
128
+aVF and - I
right axis deviation
129
-aVF and - I
extreme right axis deviation
130
-aVF and + I
left axis deviation
131
Causes of left axis deviation
left heart enlargement (dilation or hypertrophy)
conduction defects
acute MI on right side to shift axis left
132
Causes of right axis deviation
right heart enlargement
conduction defect of right ventricle or posterior left bundle branch
acute MI on left side
133
First degree heart block features
long PR interval, slowed conduction though AV node, rate and rhythm normal
134
Second degree heart block features
Some impulses are not transmitted through the AV node
1. Wenchelback: progressive prolongation of the PR interval until beat is missed and the cycle begins
2: PR interval consistent, but rhythm can be steady or unsteady depending on ratio (2:1, 3:1, etc)
135
Third degree heart block features
complete dissociation between P waves and QRS complexes
| impulses are not transmitted through AV node
136
A flutter features
very fast atrial rate
| rhythm still coordinated and normal
137
AF features
uncoordinated atrial conduction
lack of a coordinated conduction results in no atrial contraction
unsteady rhythm and no p waves
138
WPW features
short PR interval, steady rhythm, and normal rate, slurred upstroke of the R wave widened QRS complex
cardiac impulse can travel retrograde fashion to atria over the accessory pathway and initiate a reentrant tachycardia
139
ST elevation is from
transmural infarct or prinzmetal angina (coronary vasospasm)
140
ST depression is from
subendochardial ischemia or exertion (stable) angina
141
Hyperkaelaemia _______ rate of repolarization, resulting in _____________
increases rate of depolarization, resulting in sharp-spiked T waves and a shortened QT interval
142
Hypokalaemia _______ rate of repolarization, resulting in _____________
decreases, U waves and a prolonged QT interval
143
Hypercalcemia _________ QT interval
decreases
144
Hypocalcemia _________ QT interval
increases
145
A sarcomere is debarked by
2 z lines
146
Function of the T-tubule
membranes are extensions of the surface membrane; therefore, the interiors of the T tubules are part of extracellular compartment
147
Function of terminal cistern
the sarcoplasmic reticulum is part of the internal membrane system, one function of which is to store calcium, in skeletal muscle, most calcium is stored close to T-tubule system
148
What does tropomyosin do?
blocks myosin binding sites on actin
149
3 subunits of troponin
troponin T (binds tropomyosin), troponin I (binds to actin and inhibits contraction) and troponin C (binds to calcium)
150
Myosin has what activity? What does this do?
ATPase, splitting ATP puts myosin in a high energy state, increases myosin affinity for actin
once myosin binds to actin, the chemical energy is transferred to mechanical energy, causing myosin to pull on the actin filament = power stroke!
151
If force generated by power stroke is sufficient to move the load, the muscle _________
shortens (isotonic)
152
If force generated by power stroke is not sufficient to move the load, the muscle _________
doesn't shorten (isometric)
153
Cross-bridge cycling starts when...
Free calcium is available and attaches to troponin, which in turn moves tropomyosin so that myosin binds to actin, contraction is the continuous cycling of cross-bridges
154
What is ATP required for in the cross bridge?
for breaking the cross bridge but not for linking
155
How long does cross-bridge cycling continue for?
withdrawal of Ca2+: cycling stops at position 1 (normal resting muscle)
ATP is depleted: cycling stops at position 3 (rigor mortis)
156
2 key receptors involved in the flux Ca2+ from the SR into the cytosol
dihyroppyridine DHP and ryanodine RyR
157
DHP function
is a voltage-gated Ca2+ channel located in the sarcolemmal membrane
Ca2+ doesn't flux through this receptor, rather DHP functions as a voltage sensor,
DHP blocks RyR
CYTOSOL
158
RyR function
calcium channel on SR membrane, when the muscle is in the resting state, RyR is blocked by DHP
159
Skeletal muscle sequence
1. AP is initiated in NMJ
2. AP travels down T-tubule
3. Voltage change causes shift in DHP, removing block from RyR
4. removal of DHP block allows Ca2+ to diffuse into the cytosol
5. rise in systolic Ca2+ opens more RyR channels (CICR)
6. Ca2+ binds to troponin-C = cross bridge
7. Ca2+ is pumped back into SR by calcium ATPase called SERCA
8. systolic Ca2+ falls causing tropomyosin to once again cover actins binding site for myosin and muscle relaxes
160
Contraction-relaxation states are determined by _________
systolic levels of Ca2+
161
Source of Ca2+ in skeletal muscle
solely from cells SR, so no extracellular Ca2+ is involved
162
Cardiac and skeletal muscle similarities
```
both are striated
rise in Ca2+ initiates cross-bridge cycling
ATP
SERCA
both have RyR and therefore CICR
```
163
Dysfunction in the titan protein has been associated with _____________
dilated and restrictive cardiomyopathies
164
Differences between skeletal and cardiac
extracellular Ca2+ is involved in cardiac contractions (this is what causes CICR)
magnitude of SR Ca2+ release can be altered in cardiac, but not skeletal muscle
cardiac has gap junctions
cardiac has SERCA and a Na-Ca2+ exchanger, skeletal only has SERCA
165
How does smooth muscle differ from skeletal and cardiac? Why?
actin binds to myosin via the phosphorylation by MLCK, this is because smooth muscle lacks tropomyosin, troponin, and titin
166
What does increasing IP3 in smooth muscle do?
evokes calcium efflux from SR, IP3 is increased by an agonist binding a Gq receptor (IP3 +DAG = Ca2+)
167
How does MLCK become activated?
Ca-Calmodulin binding, which in turn phosphorylates MLC
168
How is actin dissociated from myosin in smooth muscle?
ATP
169
The greater the preload the _______ stretch of the sarcomere, the greater the preload, the _______ passive tension in the muscle
greater, greater
170
Passive tension
produced by preload
171
Active tension
produced by cross-bridge cycling
172
Total tension
sum of active and passive tension
173
Maximum tension occurs when?
0 preload (no tension to start with - resting)
174
Maximum velocity of shortening occurs when? Why?
0 afterload on the muscle, afterload decreases velocity
175
When afterload exceeds maximum force by muscle, what happens?
Isometric contraction
176
What is Vmax determined by?
muscles ATPase activity
177
white vs red muscle
white: large mass per motor unit, high ATPase activity, high capacity for anaerobic glycolysis, low myoglobin
red: small mass per motor unit, lower ATPase activity, high capacity for aerobic metabolism, high myoglobin
178
pulmonary vs systemic blood (artery/vein and o2/co2 composition)
pulmonary artery = systemic vein composition
| pulmonary vein = systemic artery composition (high o2, low co2)
179
Poiseuille equation
```
Q = (P1-P2)/R
Q= flow
P1: upstream pressure
P2: pressure at the end of the segment
R: resistance of vessels between P1 and P2
```
180
What are the units of resistance?
mmHg/ml/min
181
What is the most important factor determining resistance?
Vessel radius
182
Where is the largest pressure drop? What does this mean?
Arterioles, highest resistance segment
183
What is hematocrit?
Volume of blood that is RBCs
184
What is the bloods prime determinant of viscosity?
hematocrit
185
Mean linear velocity is equal to what? Why is this important?
Flow/cross-sectional-area
Important because velocity is therefore high in aorta and low in the capillaries (because cross sectional area is low in aorta and high in capillaries)
186
Velocity vs blood flow
velocity is a rate (cm/sec)
187
Laminar flow, what is it and where is the highest velocity?
flow in layers, it occurs throughout the normal cardiovascular system, excluding flow in the heat
highest velocity is in the centre of the tube
188
Turbulent flow, what is it and what are its features?
Non layered flow, it creates murmurs, these are heard as bruits in vessels with severe stenosis
189
Which produces more resistance, laminar flow or turbulent flow?
Turbulent
190
Reynold's number?
<2000= laminar flow
>2000= turbulent flow
= (diameterxvelocityxdesnity)/viscosity
191
What increases Reynolds number?
increasing diameter, increasing velocity, decreasing blood viscosity, stenosis
192
Is resistance less in series or parallel circuits? How is this relevant?
less in parallel, this matters because the blood flow to all of the organs is the result of parallel branches off of the aorta. the total resistance of systemic circulation is less than if the organs were in series blood flow
193
What is compliance of a vessel? vs elasticity
How easily it is stretched, opposite from elasticity, a vessel has a high elasticity ( large tendency to rebound from a stretch) has a low compliance
194
compliance of systemic veins vs arteries
veins are 20 times more compliant
195
LaPlace relationship
```
T = Pr
Wall tension (is proportional to) pressurexradius
```
196
Which vessel has the greatest wall tension?
Aorta
197
What is the importance of wall tension?
In aneurysms or dilated heart failure, because the pressure is the same throughout but the radius of the aneurysm or the dilated heart is greater, there is greater wall tension
198
Preload definition
load on the muscle in a relaxed state
199
Preload is measured by (i.e. in the left ventricle)
Left EDV
| left end diastolic pressure
200
What causes a gain in contractility? Loss?
```
Calcium
Myocyte dysfunction (calcium doesn't explain losses in contractility)
```
201
What happens as a result of increased contractility?
Increased change in pressure (increased rate of pressure development)
increased peak left ventricular pressure due to a more forceful contraction
increased rate of relaxation due to increased rate of calcium sequestion
decreased systolic interval due to effects of pressure development and relaxation
202
Sympathetic activity on systolic and diastolic intervals
decrease both
systolic: contractility
diastolic: heart rate effect
203
SVR aka
TPR
204
Afterload increased in 3 main situations
when aortic pressure is increased
when SVR is increased
in aortic stenosis
205
What is ejection fraction equation and what is normal value
SV/EDV
| >55% in a normal heart
206
What happens in systolic dysfunction?
An abnormal reduction in ventricular emptying due to impaired contractility or excessive afterload
207
What happens in diastolic dysfunction>
a decrease in ventricular compliance (the ventricle is stiffer) reduced compliance causes an elevated diastolic pressure for any given volume. EDV is often reduced, but compensatory mechanisms may result in a normal EDV
208
What happens during a pressure overload?
i.e. hypertension and aortic stenosis
there is no decrease in CO initially or increase in preload
to attempt to normalize wall tension, the ventricle develops a concentric hypertrophy
209
Examples of a volume overload on the left ventricle include... What happens?
Mitral and aortic insufficiency and patent ductus arterioles, Can precipitate heart failure, due to the LaPlace relationship, a dilated left ventricle must develop a greater wall tension to produce the same ventricular pressures = LV hypertrophy
210
3 types of cardiomyopathy
Dilated
Restrictive
Hypertrophic
211
What happens in dilated cardiomyopathy?
Diastolic function remains intact and helps compensate for the chamber dilation
Compensation also includes increased sympathetic stimulation to the myocardium
Systolic dysfunction
further dilation over time = FAILURE! (mitral and tricuspid failure enhance systolic dysfunction)
212
What happens in restrictive cardiomyopathy?
Decreased ventricular compliance with diastolic dysfunction and a decrease in ventricular cavity size
systolic maintained close to normal
213
What happens in hypertrophic cardiomyopathy?
septal or left ventricular hypertrophy is unrelated to pressure load
diastolic dysfunction due to increased muscle stiffness and impaired relaxation
214
What is HOCM?
Subtype of hypertrophic cardiomyopathy , often resulting in a restriction of the ventricular outflow tract (idiopathic hypertrophic sub aortic stenosis) and pulmonary congestion
215
Parasympathetic vs sympathetic affects of baroreceptor
parasympathetic: HR
sympathetic: HR and cont., TPR, venous constriction
216
Where are baroreceptors?
carotid sinus and aortic arch
217
Activation of arterial baroreceptors inhibits
ADH
218
Are there mechanoreceptors in the heart?
Yes! They are in the walls of the heart, great veins where they empty into the right atrium, and pulmonary artery
afferent activity is relayed to the medulla via CNX
219
How do the mechanoreceptors in the heart work?
rise in volume in the heart = decrease in SNS (sympathetic) activity and increase in PNS activity
reduction in volume in heart: increase SNS activity and decrease PNS
220
2 consequences related to the fact arterioles serve as the primary site of resistance
they regulate blood flow to the capillaries
| they regulate upstream pressure, which is MAP
