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Physiology Flashcards

1
Q

What % of the body mass is water?

A

60

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2
Q

Intracellular fluid makes up _____ of total body water

A

2/3

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3
Q

Extracellular fluids makes up ____ of total body water

A

1/3

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4
Q

What is the ECF composed of?

A

3/4 is ISF

1/4 is PV

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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

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6
Q

What separates ISF from vascular volume?

A

capillary membranes

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7
Q

What is the difference between osmolarity and osmolality?

A 
Osmolarity = mOsm/L 
Osmolality = mOsm/kg of water
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8
Q

What is the term for a solute that does not easily cross the membrane?

A

“Effective” osmole

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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

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10
Q

What is a basic metabolic profile?

A

The common labs provided from a basic blood draw

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11
Q

What is the osmolar gap?

A

It is the difference between the measured osmolality and the estimated osmolality

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12
Q

How do we calculate the osmolar gap?

A

ECF estimated osmolality: 2(Na) mEq/L + glucose mg%/18 + urea mg%/2.8

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13
Q

What is a normal osmolar gap?

A

<15

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14
Q

Examples of loss of isotonic fluid? (3)

A

Hemorrhage, diarrhoea, vomiting

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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

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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
________ _____
| | –> | |
————— ———-

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17
Q

D-Y diagram features

A

Vertical: concentration of solute
Horizontal: left = ICF volume, right = ECF volume

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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

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19
Q

Examples of loss of hypotonic fluid?

A

Dehydration, DI, alcoholism

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20
Q

Gain of isotonic fluid example?

A

Saline

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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

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22
Q

Gain of hypotonic fluid example?

A

Hypotonic saline, water intoxication

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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

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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

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25
Q

What are the 2 primary factors stimulating aldosterone release?

A

K+

Angiotensin II

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26
Q

What are the 2 primary regulators of ADH release?

A 
Plasma osmolarity (direct)
Blood pressure/volume (indirect)
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27
Q

2 ADH receptors and function?

A 
V1 = vasoconstriction
V2 = water reabsorption
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28
Q

Is renin a hormone?

A

No, renin is an enzyme

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29
Q

What does renin do?

A

Renin converts angiotensinogen to angiotensin I, which in turn is converted to Any II by ACE

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30
Q

What are the 3 primary regulators of renin release?

A

GFR (inversely related)
Sympathetic stimulation to the kidney (via B1)
Na delivery to macula dense (inversely related)

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31
Q

In terms of pressures, what does P and pi stand for?

A 
P = hydrostatic
pi = osmotic
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32
Q

Filtration vs absorption

A

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)

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33
Q

Absorption pressures

A

piCapillary

PInterstitial

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34
Q

Filtration pressures

A

piInterstitial

Pcapillary

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35
Q

What is Pc directly related to?

A

BP, venous flow, BV

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36
Q

What protein is the biggest contributor to the piC?

A

Albumin!

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37
Q

Starling equation =

A

Qf = k [(Pc + piIF) - (PIF + piC)]

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38
Q

Positive Qf =

A

net filtration

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39
Q

Negative Qf =

A

net absorption

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40
Q

How to lymphatics contribute to the interstitial fluid volume and protein content?

A

Directly proportional to interstitial fluid pressure, thus a rise in this pressure promotes fluid movement out of the interstitium via lymphatics

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41
Q

Which veins do the lymphatics drain into?

A

Subclavian

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42
Q

Is pitting or non-pitting oedema more common?

A

Pitting

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43
Q

What is pitting oedema?

A

Pressing the affected area results in visual indentation of the skin
Responds well to diuretic therapy

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44
Q

What is non-pitting oedema?

A

Does not indent when pressing area, this occurs when interstitial oncotic forces are elevated, it does not respond well to diuretic therapy

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45
Q

What causes peripheral oedema? (all of the forces and the causes for change)

A

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

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46
Q

What is “k”?

A

Capillary permeability

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47
Q

What can pulmonary oedema lead to?

A

hypoxemia and hypercapnia

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48
Q

2 causes of pulmonary oedema (forces)

A
  1. Cardiogenic - elevated Pc (most common)

2. Non-cardiogenic - decreased permeability (ARDS)

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49
Q

What causes cardiogenic pulmonary oedema?

A

Increased left arterial pressure increases venous pressure = increased capillary pressure
Initially increased lymph flow reduces proteins and is protective
Elevated pulmonary wedge pressure

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50
Q

First sign of cardiogenic pulmonary oedema and treatment?

A

Orthopnea (dyspnea laying down)

Diuretics

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51
Q

How does non-cardiogenic pulmonary oedema happen?

A

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

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52
Q

Causes of non-cardiogenic pulmonary oedema? signs?

A

sepsis, bacterial pneumonia, trauma, ARDS

Rapid onset dyspnea, hypoxemia, and diffuse pulmonary infiltrates = respiratory failure

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53
Q

How do you calculate volume of the compartment?

A

amount of tracer/concentration of tracer in the compartment to be measured

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54
Q

Volume =

A

D/C

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55
Q

Tracer for.. Plasma, ECF, TBW

A

Albumin, inulin/sucrose/sodium, tritiated water/urea

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56
Q

Fractional concentration of RBC is also known as

A

Haematocrit

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57
Q

Blood volume =

A

Plasma volume/1-haematocrit

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58
Q

What % of body is blood volume?

A

Approx. 7%

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59
Q

What is membrane potential?

A

Separation of charge across membrane at rest

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60
Q

What is electrochemical gradient?

A

combination of 2 forces, chemical based on chemical concentration, electrical based on charge

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61
Q

What is conductance?

A

flow of an ion across membarne

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62
Q

What is an ungated ion channel?

A

always open, direction of ion move depends on EC forces

resting membrane potential!

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63
Q

What is a voltage gated channel?

A

open/closed determined by membrane potential

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64
Q

What is a ligand gated channel?

A

channel has a receptor

state of channel influenced by ligand to the receptor

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65
Q

What receptor is an exception to the 3 classes?

A

NMDA is both voltage and ligand

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66
Q

How is NMDA both ligand and voltage gated?

A

NMDA blocked by Mg2+ if Em is more negative than -70 (voltage)
NMDA ligands are glutamate and aspartate

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67
Q

What are NMDA receptors used for?

A

memory and pain transmission

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68
Q

Equilibrium is calculated via the _____ equation

A

Nerst

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69
Q

Depolarization less ____ hyper polarization more _______

A

negative

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70
Q

Hyperkalaemia ____ the cell

A

depolarizes

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71
Q

Hypokalaemia _____ the cell

A

hyper polarizes

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72
Q

What happens when the cell depolarizes?

A

nerves become excited

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73
Q

What happens when the cell hyper polarizes?

A

nerves decrease excitability

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74
Q

Na K relationship

A

2K in 3 Na out

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75
Q

3 states of a voltage gated Na+ channel

A

closed (rest), opened (activated), inactivated

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76
Q

closed state of voltage gated Na+ channel

A

activation gate closed (extracellular) and inactivation gate open (cytosol)

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77
Q

open state of Na+ channel

A

depolarization causes both channels to open

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78
Q

inactivated Na+ channel

A

activation gate open inactivation gate closed

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79
Q

What blocks fast Na+ channels?

A

extracellular Ca2+

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80
Q

what is the primary mechanism for depolarization?

A

K+ channels

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81
Q

explain what happens during an action potential

A
  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
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82
Q

absolute vs relative refractory period

A

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

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83
Q

what influences conduction velocity in nerves? (2)

A

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)

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84
Q

NMJ events (6)

A
  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
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85
Q

where does the NMJ synapse happen?

A

between axons of an alpha motor neurone and a skeletal muscle fibre

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86
Q

synaptic potentials are produced by

A

ligand gated ion channels

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87
Q

Does Ca2+ depolarize or depolarize the cell?

A

Depolarizes!

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88
Q

What is the primary mechanism for repolarization?

A

Voltage-Gated K+ channels

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89
Q

Where is the origin for the action potential of the axon? What is special about it?

A

Axon hillock - high density of fast Na+ channels

90
Q

What is excitatory post synaptic potential?

A

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
Q

Which receptors produce EPSP?

A

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
Q

What is inhibitory postsynaptic potential?

A

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
Q

IPSP receptors

A

GABA

glycine

94
Q

3 section of PNS

A

Motor (alpha motor neurons)
Parasympathetic
Sympathetic

95
Q

Alpha motor neurons bind to _____ and are ______ _______ neurons

A

Nm

large, well-myelinated

96
Q

Preganglionic parasympathetic neurons release _______ which binds to ______

A

ACh

Nn receptor

97
Q

Postganglionic parasympathetic fibres release ____ which binds to _____

A

ACh

muscarinic (G protein coupled)

98
Q

Preganglionic sympathetic neurons release______ which binds to _____

A

ACh, Nn

99
Q

Postganglionic sympathetic neurons mostly release ______ which binds to ______

A

NE

alpha and beta (1+3) receptors (G protein coupled)

100
Q

Parasympathetic pre is short/long and post is short/long

A

long, short

101
Q

Sympathetic pre is short/long and post is short/long

A

short, long

102
Q

What is myasthenia graves?

A

autoimmune condition in which antibodies are created that block the Nm receptor

103
Q

What is Lambert-eaton syndrome?

A

autoimmune condition in which antibodies are created that block the presynaptic voltage-gated Ca2+ channels

104
Q

What cells in the heart are specialized for automaticity?

A

SA node cells

105
Q

Who becomes the pacemaker if SA is damaged?

A

AV

106
Q

Besides the SA and AV nodes, which ther part of the heart exhibits spontaneous depolarizations?

A

Purkinje cells

107
Q

AV node cells are specialized for _____ conduction

A

slow

108
Q

Purkinje cells are specialized for ______ conduction

A

fast

109
Q

Why is the resting membrane potential close to K+? why?

A

potassium conductance is high in resting ventricular or atrial myocytes resulting from 2 channels

110
Q

2 K+ channels

A

undated potassium channels - always open (potential -95)

inward K+ rectifying channels -voltage gated that are open at rest, depolarization closes

111
Q

Phase 0 of action potential in a myocyte, what happens and what part of the ECG?

A

conduction velocity is directly related to rate of change in potential, stimulation of B1 increases the slops
QRS

112
Q

Plateau phase what happens and what part of the ECG?

A

depolarization opens voltage gated Ca2+ channels (L-type) and voltage gated K+ channels
ST segment

113
Q

What part of the action potential prevents tetany in cardiac muscle?

A

plateau phase

114
Q

Phase 3 of action potential in myocyte, what happens and what part of the ECG?

A

repolarization phase, T wave

115
Q

In nodal cells, what happens in phase 4?

A

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
Q

Pacemaker potential aka

A

spontaneous depolarization potential

117
Q

NE chornotropy and dromotropy

A

SA node: increased HR

AV node: increased conduction velocity through AV node

118
Q

NE in nodal cells does what?

A

NE from post-ganglionic sympathetic nerve terminals and circulating epinephrine, B1 receptors -> opens HCN and Ca2+ channels
increases slope of pacemaker potential

119
Q

ACh in nodal cells does what?

A

from post-ganglionic fibres
M2 receptor opens K+ channels and inhibits cAMP
hyperpolarizses , reduces slope

120
Q

ACh chronotropy and dromotropy

A

SA: decreased HR

AV node: decreased conduction velocity through AV node

121
Q

J wave on ECG

A

end point of the S wave, represents isoelectric point

122
Q

y axis ECG units

A

mV

123
Q

x axis ECG units

A

0.2 seconds

124
Q

What is the mean electrical axis (MEA)?

A

net direction of current flow during ventricular depolarization

125
Q

What is normal axis degrees?

A

-30 to +110 degrees

126
Q

Which 2 leads do we use to determine MEA?

A

aVF and I

127
Q

+aVF and I

A

normal

128
Q

+aVF and - I

A

right axis deviation

129
Q

-aVF and - I

A

extreme right axis deviation

130
Q

-aVF and + I

A

left axis deviation

131
Q

Causes of left axis deviation

A

left heart enlargement (dilation or hypertrophy)
conduction defects
acute MI on right side to shift axis left

132
Q

Causes of right axis deviation

A

right heart enlargement
conduction defect of right ventricle or posterior left bundle branch
acute MI on left side

133
Q

First degree heart block features

A

long PR interval, slowed conduction though AV node, rate and rhythm normal

134
Q

Second degree heart block features

A

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
Q

Third degree heart block features

A

complete dissociation between P waves and QRS complexes

impulses are not transmitted through AV node

136
Q

A flutter features

A

very fast atrial rate

rhythm still coordinated and normal

137
Q

AF features

A

uncoordinated atrial conduction
lack of a coordinated conduction results in no atrial contraction
unsteady rhythm and no p waves

138
Q

WPW features

A

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
Q

ST elevation is from

A

transmural infarct or prinzmetal angina (coronary vasospasm)

140
Q

ST depression is from

A

subendochardial ischemia or exertion (stable) angina

141
Q

Hyperkaelaemia _______ rate of repolarization, resulting in _____________

A

increases rate of depolarization, resulting in sharp-spiked T waves and a shortened QT interval

142
Q

Hypokalaemia _______ rate of repolarization, resulting in _____________

A

decreases, U waves and a prolonged QT interval

143
Q

Hypercalcemia _________ QT interval

A

decreases

144
Q

Hypocalcemia _________ QT interval

A

increases

145
Q

A sarcomere is debarked by

A

2 z lines

146
Q

Function of the T-tubule

A

membranes are extensions of the surface membrane; therefore, the interiors of the T tubules are part of extracellular compartment

147
Q

Function of terminal cistern

A

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
Q

What does tropomyosin do?

A

blocks myosin binding sites on actin

149
Q

3 subunits of troponin

A

troponin T (binds tropomyosin), troponin I (binds to actin and inhibits contraction) and troponin C (binds to calcium)

150
Q

Myosin has what activity? What does this do?

A

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
Q

If force generated by power stroke is sufficient to move the load, the muscle _________

A

shortens (isotonic)

152
Q

If force generated by power stroke is not sufficient to move the load, the muscle _________

A

doesn’t shorten (isometric)

153
Q

Cross-bridge cycling starts when…

A

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
Q

What is ATP required for in the cross bridge?

A

for breaking the cross bridge but not for linking

155
Q

How long does cross-bridge cycling continue for?

A

withdrawal of Ca2+: cycling stops at position 1 (normal resting muscle)
ATP is depleted: cycling stops at position 3 (rigor mortis)

156
Q

2 key receptors involved in the flux Ca2+ from the SR into the cytosol

A

dihyroppyridine DHP and ryanodine RyR

157
Q

DHP function

A

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
Q

RyR function

A

calcium channel on SR membrane, when the muscle is in the resting state, RyR is blocked by DHP

159
Q

Skeletal muscle sequence

A
  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
Q

Contraction-relaxation states are determined by _________

A

systolic levels of Ca2+

161
Q

Source of Ca2+ in skeletal muscle

A

solely from cells SR, so no extracellular Ca2+ is involved

162
Q

Cardiac and skeletal muscle similarities

A 
both are striated 
rise in Ca2+ initiates cross-bridge cycling 
ATP 
SERCA
both have RyR and therefore CICR
163
Q

Dysfunction in the titan protein has been associated with _____________

A

dilated and restrictive cardiomyopathies

164
Q

Differences between skeletal and cardiac

A

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
Q

How does smooth muscle differ from skeletal and cardiac? Why?

A

actin binds to myosin via the phosphorylation by MLCK, this is because smooth muscle lacks tropomyosin, troponin, and titin

166
Q

What does increasing IP3 in smooth muscle do?

A

evokes calcium efflux from SR, IP3 is increased by an agonist binding a Gq receptor (IP3 +DAG = Ca2+)

167
Q

How does MLCK become activated?

A

Ca-Calmodulin binding, which in turn phosphorylates MLC

168
Q

How is actin dissociated from myosin in smooth muscle?

A

ATP

169
Q

The greater the preload the _______ stretch of the sarcomere, the greater the preload, the _______ passive tension in the muscle

A

greater, greater

170
Q

Passive tension

A

produced by preload

171
Q

Active tension

A

produced by cross-bridge cycling

172
Q

Total tension

A

sum of active and passive tension

173
Q

Maximum tension occurs when?

A

0 preload (no tension to start with - resting)

174
Q

Maximum velocity of shortening occurs when? Why?

A

0 afterload on the muscle, afterload decreases velocity

175
Q

When afterload exceeds maximum force by muscle, what happens?

A

Isometric contraction

176
Q

What is Vmax determined by?

A

muscles ATPase activity

177
Q

white vs red muscle

A

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
Q

pulmonary vs systemic blood (artery/vein and o2/co2 composition)

A

pulmonary artery = systemic vein composition

pulmonary vein = systemic artery composition (high o2, low co2)

179
Q

Poiseuille equation

A 
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
Q

What are the units of resistance?

A

mmHg/ml/min

181
Q

What is the most important factor determining resistance?

A

Vessel radius

182
Q

Where is the largest pressure drop? What does this mean?

A

Arterioles, highest resistance segment

183
Q

What is hematocrit?

A

Volume of blood that is RBCs

184
Q

What is the bloods prime determinant of viscosity?

A

hematocrit

185
Q

Mean linear velocity is equal to what? Why is this important?

A

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
Q

Velocity vs blood flow

A

velocity is a rate (cm/sec)

187
Q

Laminar flow, what is it and where is the highest velocity?

A

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
Q

Turbulent flow, what is it and what are its features?

A

Non layered flow, it creates murmurs, these are heard as bruits in vessels with severe stenosis

189
Q

Which produces more resistance, laminar flow or turbulent flow?

A

Turbulent

190
Q

Reynold’s number?

A

<2000= laminar flow
>2000= turbulent flow
= (diameterxvelocityxdesnity)/viscosity

191
Q

What increases Reynolds number?

A

increasing diameter, increasing velocity, decreasing blood viscosity, stenosis

192
Q

Is resistance less in series or parallel circuits? How is this relevant?

A

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
Q

What is compliance of a vessel? vs elasticity

A

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
Q

compliance of systemic veins vs arteries

A

veins are 20 times more compliant

195
Q

LaPlace relationship

A 
T = Pr
Wall tension (is proportional to) pressurexradius
196
Q

Which vessel has the greatest wall tension?

A

Aorta

197
Q

What is the importance of wall tension?

A

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
Q

Preload definition

A

load on the muscle in a relaxed state

199
Q

Preload is measured by (i.e. in the left ventricle)

A

Left EDV

left end diastolic pressure

200
Q

What causes a gain in contractility? Loss?

A 
Calcium
Myocyte dysfunction (calcium doesn't explain losses in contractility)
201
Q

What happens as a result of increased contractility?

A

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
Q

Sympathetic activity on systolic and diastolic intervals

A

decrease both

systolic: contractility
diastolic: heart rate effect

203
Q

SVR aka

A

TPR

204
Q

Afterload increased in 3 main situations

A

when aortic pressure is increased
when SVR is increased
in aortic stenosis

205
Q

What is ejection fraction equation and what is normal value

A

SV/EDV

>55% in a normal heart

206
Q

What happens in systolic dysfunction?

A

An abnormal reduction in ventricular emptying due to impaired contractility or excessive afterload

207
Q

What happens in diastolic dysfunction>

A

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
Q

What happens during a pressure overload?

A

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
Q

Examples of a volume overload on the left ventricle include… What happens?

A

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
Q

3 types of cardiomyopathy

A

Dilated
Restrictive
Hypertrophic

211
Q

What happens in dilated cardiomyopathy?

A

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
Q

What happens in restrictive cardiomyopathy?

A

Decreased ventricular compliance with diastolic dysfunction and a decrease in ventricular cavity size
systolic maintained close to normal

213
Q

What happens in hypertrophic cardiomyopathy?

A

septal or left ventricular hypertrophy is unrelated to pressure load
diastolic dysfunction due to increased muscle stiffness and impaired relaxation

214
Q

What is HOCM?

A

Subtype of hypertrophic cardiomyopathy , often resulting in a restriction of the ventricular outflow tract (idiopathic hypertrophic sub aortic stenosis) and pulmonary congestion

215
Q

Parasympathetic vs sympathetic affects of baroreceptor

A

parasympathetic: HR
sympathetic: HR and cont., TPR, venous constriction

216
Q

Where are baroreceptors?

A

carotid sinus and aortic arch

217
Q

Activation of arterial baroreceptors inhibits

A

ADH

218
Q

Are there mechanoreceptors in the heart?

A

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
Q

How do the mechanoreceptors in the heart work?

A

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
Q

2 consequences related to the fact arterioles serve as the primary site of resistance

A

they regulate blood flow to the capillaries

they regulate upstream pressure, which is MAP

Exam (6 decks)

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