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1

Factors that affect rate of diffusion

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

2

Conditions that increase membrane thickness

Lung fibrosis, pulmonary edema, pneumonia, membranous glomerulonephritis

3

Conditions that affect surface area of the membrane

Exercise (increases SA), emphysema (decreases SA)

4

Osmoles Vs. mole Vs. mEq

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

5

Characteristics of protein-mediated transport

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

6

Types of protein transport

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

7

Primary active transport

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

8

Secondary active transport

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

9

Constitutive endocytosis

Vesicles are continuously fusing with the cell membrane

10

Receptor-mediated endocytosis

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

11

Simple diffusion curve in a graph

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

12

Facilitated diffusion curve in a graph

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

13

Amount of total body water

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

14

Amount of intracellular fluid

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

15

Amount of extracellular fluid

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

16

Amount of interstitial fluid

2/3 of ECF. 14 L --> 10 L ISF

17

Amount of plasma volume

1/3 of ECF. 14 L --> 4 L plasma

18

Effective osmolarity

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

19

Capillary membranes

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

20

Isotonic fluid loss diagram

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

21

Loss of hypotonic fluid diagram (hypovolemia)

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

22

Gain of hypertonic fluid diagram

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

23

Gain of hypotonic fluid diagram

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

24

Gain of isotonic fluid diagram

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

25

Loss of hypertonic fluid diagram

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

26

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

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

27

↓ECF, ↓osmolarity, ↑ICF

Loss of hypertonic fluid or hyponatremic hypovolemia. Aldosterone deficiency.

28

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

Loss of hypotonic fluid or hypernatremic hypovolemia. Cause: Dehydration

29

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

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

30

↑ECF, no change in ICF or osmolarity

Gain of isotonic fluid. Cause: isotonic saline infusion

31

↑ECF, ↓osmolarity, ↑ICF

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

32

↑ECF, ↑osmolarity, ↓ICF

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

33

Volume of distribution formula

Vd = Amount given or dose / Concentration

34

Tracer to measure plasma volume

Not permeable to capillaries - albumin

35

Tracer to measure ECF

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

36

Tracer to measure total body water

Permeable to capillaries and membranes - tritiated water, urea

37

Blood volume Vs. plasma volume

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

38

Effect of urea solution on cell volume

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

39

Equilibrium potential

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

40

Conductance

Permeability to an ion

41

Electrochemical gradient

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

42

Types of channels

Ungated, voltage-gated, ligand-gated

43

↑[K]o

Depolarization

44

↓[K]o

Hyperpolarization

45

↑gK

Hyperpolarization

46

↓gK

Depolarization

47

↑[Na]o

Depolarization

48

↓[Na]o

Hyperpolarization

49

↑gNa

Depolarization

50

↑[Cl]o

Hyperpolarization

51

↓[Cl]o

Depolarization

52

↑gCl

Depolarization

53

Characteristics of sub-treshold potentials

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

54

Characteristics of action potentials

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

55

Factors that affect conduction velocity of the action potential

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

56

Absolute refractory period

No stimulus can depolarize the cell

57

Relative refractory period

A large stimulus can depolarize the cell

58

Neuromuscular transmission

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

59

Excitatory postsynaptic potentials

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

60

Inhibitory postsynaptic potentials

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

61

Electrical synapse

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

62

Sarcomere A band

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

63

Sarcomere H zone

Contains thick myosin filaments. Shortens during contraction.

64

Sarcomere I band

Contains thin actin filaments. Shortens during contraction.

65

Sarcomere Z line

Within the A band.

66

Sarcomere M line

Within the H zone.

67

Actin

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

68

Myosin

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.

69

Tropomyosin

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

70

Troponin

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

71

What happens if calcium is removed from sarcoplasmic reticulum?

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

72

Rigor mortis

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

73

Muscle contraction steps

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.

74

Myosin ATPase

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

75

Sarcoplasmic calcium-dependent ATPase

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

76

Source of calcium for skeletal muscle contraction

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

77

Source of calcium for heart and smooth muscle contraction

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

78

Tetanus

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

79

Preload

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

80

Afterload

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

81

What is the best measure of preload?

Sarcomere length

82

Preload-length tension curve

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

83

Isometric contraction

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

84

How is active tension produced?

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.

85

Total tension

Passive (preload) tension + active (afterload) tension

86

Active tension curve

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

87

What is L0?

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

88

Isotonic contraction

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

89

Most energy demanding phase of cardiac cycle

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

90

Relationship between load, muscle force and muscle velocity

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

91

Regulation of skeletal muscle force and work

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

92

Regulation of cardiac and smooth muscle force and work

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

93

Characteristics of white muscle

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

94

Characteristics of red muscle

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

95

Characteristics of skeletal muscle

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

96

Characteristics of cardiac muscle

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.

97

Characteristics of smooth muscle

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

98

Pressure in the right ventricle

25/0 mmHg

99

Pressure in the pulmonary artery

25/8 mmHg

100

Mean pulmonary artery pressure

15 mmHg

101

Pulmonary capillary pressure

7-9 mmHg

102

Pulmonary venous pressure

5 mmHg

103

Left atrium pressure

5-10 mmHg

104

Left ventricle pressure

120/0 mmHg

105

Aortic pressure

120/80 mmHg

106

Mean arterial blood pressure

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

107

Skeletal muscle capillary pressure

30 mmHg

108

Renal glomerular capillary pressure

45-50 mmHg

109

Peripheral vein pressure

15 mmHg

110

Right atrium pressure (central venous)

0 mmHg

111

Systemic ciruit Vs. pulmonary system

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

Highest resistance segment of the systemic circulation

Arterioles. Also responsible for greatest pressure drop.

113

Largest and smallest cross-sectional areas of the systemic circuit

Largest: capillaries; smallest: aorta

114

Fastest and slowest velocities in the systemic circuit

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

115

Largest blood volumes in the cardiovascular system

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

116

Poiseuille equation

Q = P1 - P2 / R;

117

Determinants of resistance

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

118

Reynolds number

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

119

Vessel with the most turbulent flow

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

120

Features of a series circuit

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

↓ resistance, ↑ capillary flow, ↑ capillary pressure

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

122

↑ resistance, ↓ capillary flow, ↓ capillary pressure

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

123

↓ resistance, ↑ capillary flow, ↓ capillary pressure

Venous dilation - ↑ metabolism

124

↑ resistance, ↓ capillary flow, ↑ capillary pressure

Venous constriction - physical compression, ↑ sympathetic

125

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

↑ arterial pressure - ↑ CO, volume expansion

126

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

↓ arterial pressure - ↓ CO, hemorrhage, dehydration

127

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

↑ venous pressure - CHF, physical compression

128

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

↓ venous pressure - hemorrhage, dehydration

129

Characteristics of parallel circuits

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

Parallel circuits with greatest resistance

Coronary > cerebral > renal > pulmonary

131

What happens if a parallel circuit is added?

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

132

What happens if a parallel cuircuit is removed?

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

133

Wall tension

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

134

Factors that increase systolic pressure

↑ stroke volume, ↓ HR, ↓ compliance

135

Factors that decrease systolic pressure

↓ stroke volume, ↑ HR, ↑ compliance

136

Factors that decrease diastolic pressure

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

137

Factors that increase diastolic pressure

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

138

Factors that increase pulse pressure

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

139

Determinants of mean arterial pressure

MAP = CO x TPR

140

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

MAP increases and CO decreases

141

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

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

142

Hemodynamic changes in hemorrhage

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

Hemodynamic changes during exercise

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

144

Hemodynamic changes due to gravity

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

145

Effects of inspiration on blood flow

↓ 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

Effects of expiration on blood flow

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

147

What factor controls blood flow to capillaries?

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

148

What factors affect capillary exchange?

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

When does the rate of uptake become perfusion-limited?

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

150

When does the rate of uptake becom diffusion-limited?

When concentration between capillary and tissue are not in equilibrium.

151

What forces favor reabsorption?

Capillary oncotic pressure and interstitial hydrostatic pressure

152

What forces favor capillary filtration?

Capillary hydrostatic pressure and interstitial oncotic pressure

153

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

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

154

Conditions that affect capillary hydrostatic pressure

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

155

Conditions that affect capillary oncotic pressure

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

156

Conditions that affect interstitial oncotic pressure

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

157

Conditions that affect insterstitial hydrostatic pressure

Increased by negative intrathoracic pressure in ARDS

158

Fick principle

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

159

Intrinsic autoregulation of blood flow

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

160

Metabolic hypothesis of autoregulation

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

161

Tissues that have autoregulation of blood flow

Cerebral, coronary and exercising skeletal muscle circulations

162

Extrinsic regulation of blood flow

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

163

Tissues that have extrinsic regulation of blood flow

Resting skeletal muscle, skin

164

Lowest venous PO2 in the body

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

165

Factors that control coronary circulation

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

Factors that control cerebral blood flow

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

Factors that control cutaneous blood flow

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

168

Highest venous PO2 in the body

Renal circulation

169

Factors that control renal circulation

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

170

Characteristics of pulmonary circuit

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

171

Pulmonary response to exercise

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

172

Pulmonary response to hemorrhage

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

173

Fetal circulation: percent O2 saturation in umbilical vein

80% O2 saturation

174

Fetal circulation: percent O2 saturation in inferior vena cava

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

175

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

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

176

Fetal circulation: percent O2 saturation in superior vena cava

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

177

Fetal circulation: percent O2 saturation in right ventricle

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

Fetal circulation: percent O2 saturation in ascending aorta

Contains blood from inferior vena cava --> 67%

179

Fetal circulation: percent O2 saturation in brachiocephalic trunk

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

180

Fetal circulation: percent O2 saturation in descending and abdominal aorta

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

181

Ion channels present in the heart

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

182

Voltage-gated Na channels of the heart

Open and close fast upon depolarization of the membrane

183

Voltage-gated calcium channels of the heart

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

184

Inward rectifying iK1 channels of the heart

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

185

Delayed rectifying iK channels of the heart

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

186

Phase 0 of the ventricular action potential

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

187

Phase 1 of the ventricular action potential

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

188

Phase 2 of the ventricular action potential

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

189

Phase 3 of the ventricular action potential

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

190

Phase 4 of the ventricular action potential

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

191

Why can't the heart be tetanized?

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

192

How do premature ventricular depolarizations occur?

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

193

Funny current

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

Phase 0 of SA nodal cells

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

195

Phase 3 of SA nodal cells

Repolarization due to ↑ gK.

196

Phase 4 of SA nodal cells

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

197

Effects of sympathetics on pacemaker cells

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

198

Effects of parasympathetics on pacemaker cells

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

199

Fastest conducting cells of the heart

Purkinje cells

200

Slowest conducting cells of the heart

SA nodal cells

201

PR interval

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

202

QRS complex

Ventricular depolarization - should be less than 0.12 seocnds.

203

QT interval

Indicates ventricular refractorieness. Normal between 0.35 - 0.44 seconds.

204

Effect of hypercalcemia in ECG

Shortened QT interval (< 0.35 seconds).

205

Effect of hypocalcemia in ECG

Prolonged QT interval (> 0.44 seconds)

206

Drugs that shorten QT interval

Digitalis

207

Drugs that prolong QT interval

Quinidine, procainamide

208

Effect of intracerebral hemorrhage in ECG

Inverted T waves with prolonged QT interval

209

ST segment

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

210

First-degree block in ECG

Slowed conduction through AV node. PR interval > 200 msec

211

Second-degree block in ECG

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

212

Third-degree block in ECG

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

213

Sinus rhythms

Normal, bradycardia or tachychardia

214

Atrial flutter

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

215

Atrial fibrillation

No discernable P waves, irregular QRS

216

Ventricular fibrillation

No identifiable waves. Chaotic, erratic rhythm.

217

Causes of left axis deviations

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

218

Causes of right axis deviations

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

219

Initial AMI in ECG

ST segment depression, prominent Q waves, T wave inversion

220

AMI in ECG

ST segment elevation, T wave inversion, prominent Q waves

221

Resolving AMI in ECG

Baseline ST, inverted T waves, prominent Q waves

222

Stable infarct in ECG

Prominent Q waves

223

Indices of left ventricular preload

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

224

Sarcomere length in skeletal muscle Vs. heart muscle

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

Factors that increase slope of cardiac function curve

↑ inotropy, ↑ heart rate, ↓ afterload

226

Factors that decrease slope of cardiac function curve

↓ inotropy, ↓ heart rate, ↑ afterload

227

Factors that shift vascular function curve up and to the right

↑ blood volume, ↓ venous compliance

228

Factors that shift vascular function curve down and to the left

↓ blood volume, ↑ venous compliance

229

Factors that increase slope of vascular function curve

↓ SVR

230

Factors that decrease slope of cardiac function curve

↑ SVR

231

What is contractility and what influences it?

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

232

Indices of contractility

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

233

Changes to the action potential induced by increased contractility

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

234

Changes to the action potential induced by heart rate

↓ diastolic interval

235

Cardiac function curve in hemorrhage

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

236

Cardiac function curve in excersice

↑ contractility (up, same preload)

237

Cardiac function curve in volume overload

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

238

Cardiac function curve in CHF

↓ contractility (down); ↑ preload (right)

239

Afterload

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

240

Parasympathetic innervation of SA and AV nodes

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

241

Effect of inspiration on heart rate

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

242

Baroreceptor reflex

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

Acute reflex changes when blood pressure increases

↑ afferent baroreceptors --> ↑ parasympathetic, ↓ sympathetic

244

Acute reflex changes when blood pressure decreases

↓ afferent baroreceptors --> ↓ parasympathetic, ↑ sympathetic

245

Acute reflex changes with occlusion of the carotid

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

246

Acute reflex changes with a carotid massage

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

247

Acute reflex changes if baroreceptor afferents are cut

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

248

Acute reflex changes in orthostatic hypotension or fluid loss

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

249

Acute reflex changes in volume overload

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

250

S1 heart sound

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

251

S2 heart sound

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

252

Isovolumetric contraction

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

253

Ejection phase

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

254

Isovolumetric relaxation

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

255

Filling phase

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

256

Stroke volume

EDV - ESV

257

Ejection fraction

Stroke volume / EDV

258

a wave of the venous pulse

Produced by contraction of the right atrium

259

c wave of the venous pulse

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

260

v wave of the venous pulse

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

261

y wave of the venous pulse

Opening of tricuspid valve and atrial emptying

262

Aortic stenosis

Increase in afterload. Systolic murmur, concentric hypertrophy.

263

Aortic insufficiency

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

264

Mitral stenosis

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

265

Mitral insufficiency

↑ atrial volume and pressure; systolic murmur