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Step 1 Complete > Physio 1 USMLE > Flashcards

Physio 1 USMLE Flashcards

1
Q

Factors that affect rate of diffusion

A

Concentration, surface area, solubility, membrane thickness, molecular weight

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2
Q

Conditions that increase membrane thickness

A

Lung fibrosis, pulmonary edema, pneumonia, membranous glomerulonephritis

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3
Q

Conditions that affect surface area of the membrane

A

Exercise (increases SA), emphysema (decreases SA)

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4
Q

Osmoles Vs. mole Vs. mEq

A

150 mM of NaCl = 300 mOsm. Moles yield osmoles. 10 mOsm Ca++ = 20 mEq

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5
Q

Characteristics of protein-mediated transport

A

More rapid than diffusion, transport can be saturated (Tm), is chemically specific, substances compete for transporter

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6
Q

Types of protein transport

A

Facilitated (down a concentration gradient), active (against gradient, requires ATP)

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7
Q

Primary active transport

A

ATP consumed directly by the transporter. E.g. Na/K countertransport

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8
Q

Secondary active transport

A

Depends indirectly on ATP. E.g. Na/glucose cotransporter in the renal tubule depends on Na/K countertransporter

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9
Q

Constitutive endocytosis

A

Vesicles are continuously fusing with the cell membrane

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10
Q

Receptor-mediated endocytosis

A

The ligand binds receptor near clathrin-coated pits. More rapid and specific than constitutive endocytosis.

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11
Q

Simple diffusion curve in a graph

A

Linear. Slope increases if diffusion area or concentration increases. Slope decreases if membrane thickness increases

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12
Q

Facilitated diffusion curve in a graph

A

Reaches a plateau which represents Tm. Adding more transporters raises Tm, shifts curve up and right.

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13
Q

Amount of total body water

A

60% of weight in kg. 70kg = 42 L

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14
Q

Amount of intracellular fluid

A

2/3 of total body water or 40%. 42 L –> 28 L ICF

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15
Q

Amount of extracellular fluid

A

1/3 of total body water or 20%. 42 L –> 14 L ECF

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16
Q

Amount of interstitial fluid

A

2/3 of ECF. 14 L –> 10 L ISF

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17
Q

Amount of plasma volume

A

1/3 of ECF. 14 L –> 4 L plasma

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18
Q

Effective osmolarity

A

Represented by non-penetrating solutes such as Na. If effective osmolarity increases, cells shrink and vice versa.

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19
Q

Capillary membranes

A

Are freely permeable to substances dissolved in plasma except proteins. Separate ISF and plasma.

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20
Q

Isotonic fluid loss diagram

A

Decreased ECF, no change in ICF. Causes: hemorrhage, isotonic urine, diarrhea, vomiting

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21
Q

Loss of hypotonic fluid diagram (hypovolemia)

A

Decreases ECF and ICF, increases osmolarity. Causes: dehydration, sweating, diabetes insipidus.

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22
Q

Gain of hypertonic fluid diagram

A

Increases osmolarity and ECF, decreases ICF. Causes: salt tablets, mannitol, hypertonic saline, aldosterone

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23
Q

Gain of hypotonic fluid diagram

A

Decreases osmolarity, increases ECF and ICF. Causes: SIADH, drinking tap water, primary polydipsia.

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24
Q

Gain of isotonic fluid diagram

A

Osmolarity stays the same, ECF increases. Causes: isotonic saline infusion.

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25
Q

Loss of hypertonic fluid diagram

A

Osmolarity decresaes, ECF decreases, ICF increases. Causes: mineralocorticoid deficiency

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26
Q

↓ECF, no change in osmolarity or ICF, isotonic urine

A

Loss of isotonic fluid. Causes: hemorrhage, diarrhea, vomiting

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27
Q

↓ECF, ↓osmolarity, ↑ICF

A

Loss of hypertonic fluid or hyponatremic hypovolemia. Aldosterone deficiency.

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28
Q

↓ECF, ↑osmolarity, ↓ICF, little concentrated urine

A

Loss of hypotonic fluid or hypernatremic hypovolemia. Cause: Dehydration

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29
Q

↓ECF, ↑osmolarity, ↓ICF, lots of diluted urine

A

Loss of hypotonic fluid or hypernatremic hypovolemia. Cause: diabetes insipidus

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30
Q

↑ECF, no change in ICF or osmolarity

A

Gain of isotonic fluid. Cause: isotonic saline infusion

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31
Q

↑ECF, ↓osmolarity, ↑ICF

A

Gain of hypotonic fluid or hyponatremic hypervolemia. Causes: hypotonic saline, SIADH, tap water.

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32
Q

↑ECF, ↑osmolarity, ↓ICF

A

Gain of hypertonic fluid. Causes: salt tablets, mannitol, aldosterone excess

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33
Q

Volume of distribution formula

A

Vd = Amount given or dose / Concentration

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34
Q

Tracer to measure plasma volume

A

Not permeable to capillaries - albumin

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35
Q

Tracer to measure ECF

A

Permeable to capillaries but not membranes - inulin, mannitol, sodium, sucrose

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36
Q

Tracer to measure total body water

A

Permeable to capillaries and membranes - tritiated water, urea

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37
Q

Blood volume Vs. plasma volume

A

Blood volume is plasma plus RBC –> plasma volume / 1-Hct

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38
Q

Effect of urea solution on cell volume

A

If urea is the only solute, effective osmolarity is 0 –> cell swells.

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39
Q

Equilibrium potential

A

Electrical force required to balance the chemical force of an unequeal concentration of ions

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40
Q

Conductance

A

Permeability to an ion

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41
Q

Electrochemical gradient

A

Exists when the electrical and/or chemical forces are not balanced. Its what determines difussion of the ion.

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42
Q

Types of channels

A

Ungated, voltage-gated, ligand-gated

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43
Q

↑[K]o

A

Depolarization

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44
Q

↓[K]o

A

Hyperpolarization

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45
Q

↑gK

A

Hyperpolarization

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46
Q

↓gK

A

Depolarization

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47
Q

↑[Na]o

A

Depolarization

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48
Q

↓[Na]o

A

Hyperpolarization

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49
Q

↑gNa

A

Depolarization

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50
Q

↑[Cl]o

A

Hyperpolarization

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51
Q

↓[Cl]o

A

Depolarization

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52
Q

↑gCl

A

Depolarization

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53
Q

Characteristics of sub-treshold potentials

A

Proportional to stimulus stregth, not propagated, decremental with distance, summation

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54
Q

Characteristics of action potentials

A

Independent of stimulus strength, propagated unchanged in magnitude, summation not possible

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55
Q

Factors that affect conduction velocity of the action potential

A

Cell diameter and amount of myelination are directly proportional to conduction velocity

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56
Q

Absolute refractory period

A

No stimulus can depolarize the cell

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57
Q

Relative refractory period

A

A large stimulus can depolarize the cell

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58
Q

Neuromuscular transmission

A

Action potential travels down axon and opens pre-synaptic Ca channels –> calcium influx –> release Ach vesicles –> Ach diffuses and attaches to nicotinic ion channels –> ↑gNa –> end-plate depolarization (local) spreads to areas with voltage-gated Na channels –> depolarization of muscle fiber

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59
Q

Excitatory postsynaptic potentials

A

Transient subtreshold depolarizations due to ↑gNa –> summation reaches axon hillock at the junction of cell body and axon –> voltage-gated Na channels depolarize the axon

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60
Q

Inhibitory postsynaptic potentials

A

↑gCl or ↑gK hyperpolarize the cell and lower treshold for depolarization

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61
Q

Electrical synapse

A

Action potential transmitted from one cell to the next via gap junctions, without synaptic delay and in both directions. Cardiac muscle, smooth muscle.

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62
Q

Sarcomere A band

A

Contains overlapping actin and myosin. Does not shorten during contraction.

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63
Q

Sarcomere H zone

A

Contains thick myosin filaments. Shortens during contraction.

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64
Q

Sarcomere I band

A

Contains thin actin filaments. Shortens during contraction.

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65
Q

Sarcomere Z line

A

Within the A band.

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66
Q

Sarcomere M line

A

Within the H zone.

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67
Q

Actin

A

Structural protein of the thin filaments, contains attachment sites for myosin cross-bridges.

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68
Q

Myosin

A

Structural protein of the thick filaments, contains cross-bridges that attach to actin. Has ATPase activity to terminate actin-myosin cross-bridges. ATP decreases actin-myosin affinity.

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69
Q

Tropomyosin

A

Part of thin filaments. Covers the actin attachment sites for the myosin cross-bridges

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70
Q

Troponin

A

Part of thin filaments, binds calcium, which moves tropomyosin out of the way exposing actin binding sites for cross-bridges.

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71
Q

What happens if calcium is removed from sarcoplasmic reticulum?

A

Muscle goes back to resting state. Removal of calcium requires ATP.

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72
Q

Rigor mortis

A

Depletion of ATP - cycling stops with myosin attached to actin - (muscle contracted).

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73
Q

Muscle contraction steps

A

Action potential travels down T-tubules –> activates dihydropiridine voltage sensors –> foot processes are pulled aways from ryanodine calcium release channels of sarcoplasmic reticulum –> calcium is released –> calcium attaches to troponin –> tropomyosin moves exposing actin binding sites for myosin cross-bridges –> myosin binds actin –> myosin ATPase breaks down cross bridges producing active tension and shortening –> contraction terminated by active pumping of Ca into the sarcoplasmic reticulum.

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74
Q

Myosin ATPase

A

Hydrolizes ATP to supply energy for active tension and shortening. ATP decreases myosin-actin affinity

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75
Q

Sarcoplasmic calcium-dependent ATPase

A

Supplies energy to terminate contraction and pump Ca back into sarcoplasmic reticulum.

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76
Q

Source of calcium for skeletal muscle contraction

A

Sarcoplasmic reticulum. No extracellular calcium is involved because it doesn’t have voltage-gated Ca channels.

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77
Q

Source of calcium for heart and smooth muscle contraction

A

Sarcoplasmic reticulum and extracellular. Cardiac and smooth muscle have voltage-gated calcium channels.

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78
Q

Tetanus

A

Multiple action potentials increase release of calcium thus increasing contraction. Muscle cells have a short refractory period.

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79
Q

Preload

A

Stretch prior to contraction. ↑ preload –> ↑ prestretch of the sarcomere –> ↑ passive tension

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80
Q

Afterload

A

The load the muscle is working against. ↑ afterload –> ↑ cross-bridge cycling –> ↑ active tension

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81
Q

What is the best measure of preload?

A

Sarcomere length

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82
Q

Preload-length tension curve

A

It’s a function of the length of the relaxed muscle. A positive parabola.

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83
Q

Isometric contraction

A

Active tension is produced but length stays the same. Afterload is greater than active tension, load not moved.

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84
Q

How is active tension produced?

A

Calcium binds troponin –> tropomysion exposes actin sites –> myosin cross-bridges bond to actin –> myosin ATPase generates energy to break cross-bridge link –> cycle repeats –> active tension. The more cross-bridges that cycle, the greater the active tension.

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85
Q

Total tension

A

Passive (preload) tension + active (afterload) tension

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86
Q

Active tension curve

A

It’s a function of the number of cross-bridges capable of cross-linking with actin. Negative parabola.

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87
Q

What is L0?

A

The optimum length to produce maximum active tension. Beyond L0, muscle is overstretched; below L0, it’s understretched.

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88
Q

Isotonic contraction

A

Muscle contracts and shortens to move the load. Occurs when total tension equals the load.

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89
Q

Most energy demanding phase of cardiac cycle

A

Isovolumetric contraction. Active tension is generated. Equivalent to isometric contraction of skeletal muscle.

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90
Q

Relationship between load, muscle force and muscle velocity

A

↑ ATPase activity –> ↑ velocity; ↑ muscle mass –> ↑ force generated; ↑ afterload –> ↓ velocity

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91
Q

Regulation of skeletal muscle force and work

A

↑ frequency of action potentials, ↑ recruitment, ↑ preload and ↑ afterload –> ↑ force and work

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92
Q

Regulation of cardiac and smooth muscle force and work

A

Factors that regulate force and work are preload, afterload and contractility (which is altered by hormones). No summation nor recruitment.

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93
Q

Characteristics of white muscle

A

Large mass, high ATPase activity (fast muscle), anaerobic glycolysis, low myoglobin

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94
Q

Characteristics of red muscle

A

Small mass, low ATPase activity (slower muscle), aerobic metabolism (mitochondria), high myoglobin.

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95
Q

Characteristics of skeletal muscle

A

Actin and myosin form sarcomeres, sarcolema lacks junctional complexes, each fiber innervated, troponin binds calcium, high ATPase activity, triadic contacts by T-tubules at A-I junctions, no calcium channels on membrane

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96
Q

Characteristics of cardiac muscle

A

Actin and myosin form sarcomeres, gap junctions, electrical syncytium, troponin binds calcium, intermediate ATPase activity, dyadic contacts by T-tubules near Z-lines, voltage-gated calcium channels.

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97
Q

Characteristics of smooth muscle

A

Actin and myosin not organized in sarcomeres, gap junctions, electrical syncytium, calmodulin binds calcium, low ATPase activity, lacks T-tubules, voltage-gated calcium channels.

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98
Q

Pressure in the right ventricle

A

25/0 mmHg

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99
Q

Pressure in the pulmonary artery

A

25/8 mmHg

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100
Q

Mean pulmonary artery pressure

A

15 mmHg

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101
Q

Pulmonary capillary pressure

A

7-9 mmHg

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102
Q

Pulmonary venous pressure

A

5 mmHg

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103
Q

Left atrium pressure

A

5-10 mmHg

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104
Q

Left ventricle pressure

A

120/0 mmHg

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105
Q

Aortic pressure

A

120/80 mmHg

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106
Q

Mean arterial blood pressure

A

(Systolic - diastolic / 3) + diastolic = 93 mmHg

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107
Q

Skeletal muscle capillary pressure

A

30 mmHg

108
Q

Renal glomerular capillary pressure

A

45-50 mmHg

109
Q

Peripheral vein pressure

A

15 mmHg

110
Q

Right atrium pressure (central venous)

A

0 mmHg

111
Q

Systemic ciruit Vs. pulmonary system

A

Cardiac output and heart rate is the same as they’re connected in series. The systemic circuit has higher resistance and lower compliance therefore work of the right ventricle is lower.

112
Q

Highest resistance segment of the systemic circulation

A

Arterioles. Also responsible for greatest pressure drop.

113
Q

Largest and smallest cross-sectional areas of the systemic circuit

A

Largest: capillaries; smallest: aorta

114
Q

Fastest and slowest velocities in the systemic circuit

A

Velocity is inversely proportional to cross-sectional area. Aorta has fastest velocity; capillaries have slowest velocity.

115
Q

Largest blood volumes in the cardiovascular system

A

Systemic veins then pulmonary system have the largest blood volume. Both represent reservoirs due to high compliance.

116
Q

Poiseuille equation

A

Q = P1 - P2 / R;

117
Q

Determinants of resistance

A

R ∝ vL / r4; if radius doubles, resistance decreases to 1/16; if radius decreases by half, resistance increases 16-fold

118
Q

Reynolds number

A

RN = diameter x velocity x density / viscosity. If > 2,000 –> turbulent flow; if < 2,000 –> laminar flow

119
Q

Vessel with the most turbulent flow

A

Aorta - has large diameter, high velocity. In anemia (↓ viscosity) –> aortic murmur

120
Q

Features of a series circuit

A

Flow is the same at all points; the total resistance is the sum of all resistances; adding a resistor decreases flow at all points and vice versa;

121
Q

↓ resistance, ↑ capillary flow, ↑ capillary pressure

A

Arteriole dilation - beta agonists, alpha blockers, ↓ sympathetic, metabolic dilation, ACEIs

122
Q

↑ resistance, ↓ capillary flow, ↓ capillary pressure

A

Arteriole constriction - alpha agonists, beta blockers, ↑ sympathetic, angiotensin II

123
Q

↓ resistance, ↑ capillary flow, ↓ capillary pressure

A

Venous dilation - ↑ metabolism

124
Q

↑ resistance, ↓ capillary flow, ↑ capillary pressure

A

Venous constriction - physical compression, ↑ sympathetic

125
Q

↑ capillary flow, ↑ capillary pressure, no change in resistance

A

↑ arterial pressure - ↑ CO, volume expansion

126
Q

↓ capillary flow, ↓ capillary pressure, no change in resistance

A

↓ arterial pressure - ↓ CO, hemorrhage, dehydration

127
Q

↓ capillary flow, ↑ capillary pressure, no change in resistance

A

↑ venous pressure - CHF, physical compression

128
Q

↑ capillary flow, ↓ capillary pressure, no change in resistance

A

↓ venous pressure - hemorrhage, dehydration

129
Q

Characteristics of parallel circuits

A

The reciprocal of the total resistance is the sum of the reciprocal of the individual resistances. Connecting a resistance in parallel lowers resistance, total resistance is always less than individual resistances.

130
Q

Parallel circuits with greatest resistance

A

Coronary > cerebral > renal > pulmonary

131
Q

What happens if a parallel circuit is added?

A

TPR decreases, pressure would decrease but a compensatory increases in CO maintains same pressure. Obesity.

132
Q

What happens if a parallel cuircuit is removed?

A

TPR increases, blood pressure increases, CO might decrease to compensate increased blood pressure.

133
Q

Wall tension

A

T ∝ Pr. In aneurysm, tension is high due to greater radius.

134
Q

Factors that increase systolic pressure

A

↑ stroke volume, ↓ HR, ↓ compliance

135
Q

Factors that decrease systolic pressure

A

↓ stroke volume, ↑ HR, ↑ compliance

136
Q

Factors that decrease diastolic pressure

A

↓ TPR, ↓ HR, ↓ stroke volume, ↓ compliance

137
Q

Factors that increase diastolic pressure

A

↑ TPR, ↑ HR, ↑ stroke volume, ↑ compliance

138
Q

Factors that increase pulse pressure

A

↑ stroke volume (systolic > diastolic); ↓ compliance (systolic increases and diastolic decreases)

139
Q

Determinants of mean arterial pressure

A

MAP = CO x TPR

140
Q

What happens to cardiac output and mean arterial pressure if TPR increases?

A

MAP increases and CO decreases

141
Q

What happens to cardiac output and TPR if mean arterial pressure decreases?

A

TPR decreases, CO decreases but then increases to compensate and maintain blood pressure

142
Q

Hemodynamic changes in hemorrhage

A

Loss of circulating volume and CO –> less firing of carotid sinus (↓ BP) –> reflex sympathetic ↑ in TPR and CO –> ↓ venous compliance –> ↑ circulating volume –> compensated CO and BP

143
Q

Hemodynamic changes during exercise

A

Dilation of arterioles –> ↓ TPR –> ↓ BP –> less firing of carotid sinus –> reflex sympathetic ↑ in CO –> ↑ BP

144
Q

Hemodynamic changes due to gravity

A

↑ venous pressure, ↑ pooling of blood in veins, ↓ circulating blood volume (CO), ↓ BP –> compensation via carotid sinus –> ↑ TPR, ↑ HR

145
Q

Effects of inspiration on blood flow

A

↓ intrapleural pressure –> ↑ venous return –> ↑ right ventricle output –> splitting of S2 –> blood in pulmonary circuit increases –> ↓ venous return to left heart –> ↓ systemic pressure –> reflex increase in HR

146
Q

Effects of expiration on blood flow

A

↑ intrapleural pressure –> ↓ venous return –> ↓ pulmonary blood volume –> ↑ output of left ventricle –> ↑ systemic pressure –> reflex bradycardia

147
Q

What factor controls blood flow to capillaries?

A

↑ resistance of arterioles –> ↓ capillary flow and pressure; ↓ resistance of arterioles –> ↑ capillary flow and pressure

148
Q

What factors affect capillary exchange?

A

Exchange is by simple diffusion only. Proteins do not cross the capillary membrane. Factors that affect diffusion rate are: surface area, membrane thickness, concentration gradient, solubility

149
Q

When does the rate of uptake become perfusion-limited?

A

When concentration of the substance reaches equilibrium between capillary and tissue. ↑ blood flow converts perfusion-limited uptake to diffusion-limited again.

150
Q

When does the rate of uptake becom diffusion-limited?

A

When concentration between capillary and tissue are not in equilibrium.

151
Q

What forces favor reabsorption?

A

Capillary oncotic pressure and interstitial hydrostatic pressure

152
Q

What forces favor capillary filtration?

A

Capillary hydrostatic pressure and interstitial oncotic pressure

153
Q

What happens to filtration in lung capillaries when intrathoracic pressure decreases?

A

↓ intrathoracic pressure promotes filtration. In ARDS –> ↓ intrathoracic pressure –> pulmonary edema

154
Q

Conditions that affect capillary hydrostatic pressure

A

Essential hypertension increases resistance and decreases capillary hydrostatic pressure. Hemorrhage decreases capillary hydrostatic pressure and promotes reabsorption.

155
Q

Conditions that affect capillary oncotic pressure

A

Increased by dehydration. Decreased by liver and renal disease and saline infusion

156
Q

Conditions that affect interstitial oncotic pressure

A

Increased by lymphatic blockage and increased capillary permeability to proteins (burns)

157
Q

Conditions that affect insterstitial hydrostatic pressure

A

Increased by negative intrathoracic pressure in ARDS

158
Q

Fick principle

A

Measures cardiac output. Flow = O2 consumption / O2 concentration difference across the organ

159
Q

Intrinsic autoregulation of blood flow

A

Resistance of arterioles is changed in order to regulate flow. No nerves or hormones involved. Independent of BP.

160
Q

Metabolic hypothesis of autoregulation

A

Tissue can produce a vasodilatory metabolite that regulates blood flow. Example adenosine in coronaries.

161
Q

Tissues that have autoregulation of blood flow

A

Cerebral, coronary and exercising skeletal muscle circulations

162
Q

Extrinsic regulation of blood flow

A

Controlled by nervous and hormonal influences. NE via β2 vasodilates, via α1 constricts (dose dependant). Angiotensin II constricts.

163
Q

Tissues that have extrinsic regulation of blood flow

A

Resting skeletal muscle, skin

164
Q

Lowest venous PO2 in the body

A

Coronary circulation due to maximal extraction of O2. To increase delivery of oxygen, flow must increase.

165
Q

Factors that control coronary circulation

A

Coronary circulation occurs in diastole and its determined by stroke work of the heart. Exercise increases volume work and coronary flow. Hypertension increases pressure work and coronary flow. Vasodilation is mediated by adenosine.

166
Q

Factors that control cerebral blood flow

A

Flow is proportional to arterial PCO2. Hypoventilation increases PCO2 and flow. Hyperventilation decreases PCO2 and flow. PO2 determines flow only if theres a large decrease in PO2.

167
Q

Factors that control cutaneous blood flow

A

↑ sympathetic tone –> constriction of arterioles –> ↓ blood flow, ↓ blood volume in veins –> ↑ velocity (↓ cross-sectional area). Increased skin temperature –> vasodilation –> heat loss

168
Q

Highest venous PO2 in the body

A

Renal circulation

169
Q

Factors that control renal circulation

A

Small changes in blood pressure invoke autoregulatory responses. Sympathetic may influence blood flow in extreme conditions (hemorrhage, hypotension)

170
Q

Characteristics of pulmonary circuit

A

Low pressure, high flow, low resistance, very compliant, hypoxic vasoconstriction.

171
Q

Pulmonary response to exercise

A

↑ CO –> ↑ pulmonary pressure –> pulmonary vessel dilation (due to high compliance) –> large ↓ resistance –> ↓ pulmonary pressure

172
Q

Pulmonary response to hemorrhage

A

↓ CO –> ↓ pulmonary pressure –> pulmonary vessel constriction –> large ↑ resistance –> less blood volume

173
Q

Fetal circulation: percent O2 saturation in umbilical vein

A

80% O2 saturation

174
Q

Fetal circulation: percent O2 saturation in inferior vena cava

A

26% O2 saturation. Mixes with hepatic vein blood –> step up to 67%

175
Q

Fetal circulation: percent O2 saturation from inferior vena cava into right atrium

A

67% O2 saturation. Blood from inferior vena cava enters right atrium and passes through foramen ovale

176
Q

Fetal circulation: percent O2 saturation in superior vena cava

A

40% O2 saturation. Mixes with blood from inferior vena cava (67%) and passes to right ventricle at 50% saturation

177
Q

Fetal circulation: percent O2 saturation in right ventricle

A

Contains blood from superior vena cava mixed with IVC –> 50% saturation. Passes through pulmonary vein and 90% is shunted through the ductus arteriosus into aorta

178
Q

Fetal circulation: percent O2 saturation in ascending aorta

A

Contains blood from inferior vena cava –> 67%

179
Q

Fetal circulation: percent O2 saturation in brachiocephalic trunk

A

Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) –> yields 65%

180
Q

Fetal circulation: percent O2 saturation in descending and abdominal aorta

A

Blood from left ventricle (67%) mixes with blood from ductus arteriousus (50%) –> yields 60%

181
Q

Ion channels present in the heart

A

Ungated K, voltage-gated fast Na, voltage-gated calcium, inward rectifying iK1, delayed rectifying iK

182
Q

Voltage-gated Na channels of the heart

A

Open and close fast upon depolarization of the membrane

183
Q

Voltage-gated calcium channels of the heart

A

Open upon depolarization, close more slowly than sodium channels. Partly responsible for the plateau (phase 2)

184
Q

Inward rectifying iK1 channels of the heart

A

Open under resting conditions, depolarization closes them, they reopen during repolarization phase.

185
Q

Delayed rectifying iK channels of the heart

A

Very slow to open with depolarization (late plateau), and close very slowly. Partly responsible for repolarization

186
Q

Phase 0 of the ventricular action potential

A

Fast Na channels open, ↑ gNa causes depolarization. Inward rectifying iK1 channels close.

187
Q

Phase 1 of the ventricular action potential

A

Slight repolarization due to transient potassium current and the closing of sodium channels

188
Q

Phase 2 of the ventricular action potential

A

Slow Ca channels open, ↑ gCa, ↓ gK. Plateau phase is due to slow calcium current and decreased K current

189
Q

Phase 3 of the ventricular action potential

A

Slow Ca channels close, the delayed rectifier iK reopen, ↑ gK. K efflux causes repolarization.

190
Q

Phase 4 of the ventricular action potential

A

Voltage-gated and ungated potassium channels are open, ↑ gK. The delayed rectifiers close but are responsible for the relative refractory period.

191
Q

Why can’t the heart be tetanized?

A

A long absolute refractory period extends through most of the contraction. Short relative refractory period.

192
Q

How do premature ventricular depolarizations occur?

A

Action potential develops during the relative refractory period, but the earlier the potential, the shorter in amplitude and duration it will be

193
Q

Funny current

A

In specialized cells of the heart. It’s a voltage-gated sodium channel the opens during repolarization and closes during depolarization. The sodium influx during phase 3 slowly depolarizes the cell towards treshold.

194
Q

Phase 0 of SA nodal cells

A

Depolarization due to opening of voltage-gated slow Ca channels.

195
Q

Phase 3 of SA nodal cells

A

Repolarization due to ↑ gK.

196
Q

Phase 4 of SA nodal cells

A

Gradually depolarizes cell towards treshold due to funny current - ↑ gNa

197
Q

Effects of sympathetics on pacemaker cells

A

Slope of phase 4 increases due to ↑ funny current and ↑ gCa. Action via β1 receptors.

198
Q

Effects of parasympathetics on pacemaker cells

A

↑ gK causing hyperpolarization and ↓ sodium funny current decreasing slope of phase 4. Effect via M2 receptors.

199
Q

Fastest conducting cells of the heart

A

Purkinje cells

200
Q

Slowest conducting cells of the heart

A

SA nodal cells

201
Q

PR interval

A

Due to conduction delay of AV node. 0.12 - 0.2 seconds or 120 to 200 miliseconds

202
Q

QRS complex

A

Ventricular depolarization - should be less than 0.12 seocnds.

203
Q

QT interval

A

Indicates ventricular refractorieness. Normal between 0.35 - 0.44 seconds.

204
Q

Effect of hypercalcemia in ECG

A

Shortened QT interval (< 0.35 seconds).

205
Q

Effect of hypocalcemia in ECG

A

Prolonged QT interval (> 0.44 seconds)

206
Q

Drugs that shorten QT interval

A

Digitalis

207
Q

Drugs that prolong QT interval

A

Quinidine, procainamide

208
Q

Effect of intracerebral hemorrhage in ECG

A

Inverted T waves with prolonged QT interval

209
Q

ST segment

A

Indicates conduction through ventricular muscle. Corresponds to plateau phase of action potential.

210
Q

First-degree block in ECG

A

Slowed conduction through AV node. PR interval > 200 msec

211
Q

Second-degree block in ECG

A

Some impulses not transmitted through AV node. Missing QRS complexes following P wave.

212
Q

Third-degree block in ECG

A

No impulses conducted from atria to ventricles. No correlation between P waves and QRS complexes.

213
Q

Sinus rhythms

A

Normal, bradycardia or tachychardia

214
Q

Atrial flutter

A

Repeated succession of atrial depolarizations. Continuous P waves. Saw-tooth appearance.

215
Q

Atrial fibrillation

A

No discernable P waves, irregular QRS

216
Q

Ventricular fibrillation

A

No identifiable waves. Chaotic, erratic rhythm.

217
Q

Causes of left axis deviations

A

Left ventricular hypertrophy or dilation, conduction defects of left ventricle, AMI on right side

218
Q

Causes of right axis deviations

A

Right ventricular hypertrophy or dilation, conduction defect of right ventricle, AMI on left side

219
Q

Initial AMI in ECG

A

ST segment depression, prominent Q waves, T wave inversion

220
Q

AMI in ECG

A

ST segment elevation, T wave inversion, prominent Q waves

221
Q

Resolving AMI in ECG

A

Baseline ST, inverted T waves, prominent Q waves

222
Q

Stable infarct in ECG

A

Prominent Q waves

223
Q

Indices of left ventricular preload

A

LVEDV, LVEDP, left atrial pressure, pulmonary venous pressure, pulmonary wedge pressure (swan-ganz)

224
Q

Sarcomere length in skeletal muscle Vs. heart muscle

A

In skeletal muscle it’s close to L0. In heart muscle, sarcomere legth is below optimal, therefore increased preload moves sarcomere legth towards optimal for maximal cross-bridge linking

225
Q

Factors that increase slope of cardiac function curve

A

↑ inotropy, ↑ heart rate, ↓ afterload

226
Q

Factors that decrease slope of cardiac function curve

A

↓ inotropy, ↓ heart rate, ↑ afterload

227
Q

Factors that shift vascular function curve up and to the right

A

↑ blood volume, ↓ venous compliance

228
Q

Factors that shift vascular function curve down and to the left

A

↓ blood volume, ↑ venous compliance

229
Q

Factors that increase slope of vascular function curve

A

↓ SVR

230
Q

Factors that decrease slope of cardiac function curve

A

↑ SVR

231
Q

What is contractility and what influences it?

A

Contractility is the force of contraction at a given preload or sarcomere length. Due to changes in intracellular calcium

232
Q

Indices of contractility

A

dp/dt (change in pressure/change in time); ejection fraction (stroke volume/EDV)

233
Q

Changes to the action potential induced by increased contractility

A

↑ slope (↑ dp/dt), ↑ peak left ventricular pressure, ↑ rate of relaxation, ↓ systolic interval

234
Q

Changes to the action potential induced by heart rate

A

↓ diastolic interval

235
Q

Cardiac function curve in hemorrhage

A

↓ preload (down); ↑ contractility to partially compensate (left)

236
Q

Cardiac function curve in excersice

A

↑ contractility (up, same preload)

237
Q

Cardiac function curve in volume overload

A

↑ preload (right); ↓ contractility (slightly down)

238
Q

Cardiac function curve in CHF

A

↓ contractility (down); ↑ preload (right)

239
Q

Afterload

A

Force that must be generated to eject blood into aorta. ↑ afterload in hypertension, ↓ afterload in hypotension. Acute ↑ in afterload –> ↓ stroke volume, ↑ EDV, ↑ preload

240
Q

Parasympathetic innervation of SA and AV nodes

A

Left vagus predominates in AV node, right vagus predominates in SA node

241
Q

Effect of inspiration on heart rate

A

Inspiration makes intrathoracic pressure more negative –> increase venous return –> Brainbridge reflex (stretch receptors in the right atrium) –> tachychardia

242
Q

Baroreceptor reflex

A

Baroreceptors in the aortic arch send afferents via vagus nerve; baroreceptors in the carotid sinus via glosopharyngeal; baroreceptor center is in the medulla. ↑ firing of baroreceptors is sensed as ↑ blood pressure –> ↑ parasympathetic, ↓ sympathetic

243
Q

Acute reflex changes when blood pressure increases

A

↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic

244
Q

Acute reflex changes when blood pressure decreases

A

↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic

245
Q

Acute reflex changes with occlusion of the carotid

A

↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

246
Q

Acute reflex changes with a carotid massage

A

↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate

247
Q

Acute reflex changes if baroreceptor afferents are cut

A

↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

248
Q

Acute reflex changes in orthostatic hypotension or fluid loss

A

↓ afferent baroreceptors –> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

249
Q

Acute reflex changes in volume overload

A

↑ afferent baroreceptors –> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate

250
Q

S1 heart sound

A

Closure of mitral and tricuspid valves; terminates ventricular filling, starts isovolumetric contraction

251
Q

S2 heart sound

A

Closure of aortic and pulmonary valves; terminates ejection phase, begins isovolumetric relaxation

252
Q

Isovolumetric contraction

A

Beginning of systole, ventricular pressure is increasing but aortic and mitral valves are closed. Most energy consumption occurs here

253
Q

Ejection phase

A

Aortic valve opens when isvolumetric contraction generates high enough pressure; ventricular volume decreases. Most work done here.

254
Q

Isovolumetric relaxation

A

Ventricular pressure decreases; volume is end-systolic volume; aortic and mitral valves are closed

255
Q

Filling phase

A

Opening of the mitral valve passes volume to ventricle followed by atrial contraction

256
Q

Stroke volume

A

EDV - ESV

257
Q

Ejection fraction

A

Stroke volume / EDV

258
Q

a wave of the venous pulse

A

Produced by contraction of the right atrium

259
Q

c wave of the venous pulse

A

Bulging of the tricuspid valve into the right atrium during ventricular contraction

260
Q

v wave of the venous pulse

A

Wave rises as the atrium is filled; terminates when the tricuspid valve opens

261
Q

y wave of the venous pulse

A

Opening of tricuspid valve and atrial emptying

262
Q

Aortic stenosis

A

Increase in afterload. Systolic murmur, concentric hypertrophy.

263
Q

Aortic insufficiency

A

↑ preload, ↑ ventricular and aortic systolic pressures, ↓ aortic diastolic pressure, diastolic murmur, eccentric hypertrophy

264
Q

Mitral stenosis

A

↑ pressure and volume in left atrium, enlargement of left atrium, diastolic murmur

265
Q

Mitral insufficiency

A

↑ atrial volume and pressure; systolic murmur

Step 1 Complete (29 decks)

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