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Physiology 1 > Heart (2) > Flashcards

Heart (2) Flashcards

1
Q

What type of action potential happens in Myocytes?

A

Fast-response AP

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2
Q

Phases of a Fast-response action potential

A

0) Upstroke
1) Partial repolarization
2) Plateau
3) Complete Repolarization
4) Em

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3
Q

Duration of a Fast response AP

A

200 ms

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4
Q

What type of action potential happens in Nodal cells?

A

Slow-response AP

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5
Q

Duration of a Slow-response AP

A

400 ms

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6
Q

Slow vs Fast-response AP

A
  • Slow does not have Phase 1&2, partial repol. & plateau
  • More negative Em in fast AP
  • Much greater slope&amplitude in fast
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7
Q

Automaticity

A

Spontaneous depolarization and generation of an AP
(SA, AV nodes)

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8
Q

(I)f

A
  • HCN4 (non-selective cation ch.)
  • Na+ in
  • Pre/pacemaker potential generation
    (<-50 hyperpol, cAMP)
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9
Q

(I)Ca T

A
  • T-type VDCC
  • Na+ & Ca2+ in
  • Initial depol.
    (Transient= temporary/short-lived)
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10
Q

(I)Ca L

A
  • L-type VDCC
  • Ca2+ in
  • Depolarization
  • ~ -30mV
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11
Q

(I)k

A
  • VG types (several)
  • K+ out
  • Repolarization
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12
Q

(I)k,ach

A
  • GIRK1 / GIRK4
  • K+ out
  • Hyperpolarization
    (Ach, Vagus n, m2-R)
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13
Q

Does HCN channel inactivate?

A

No

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14
Q

HCN channel Inhibitor

A

Ivabradine

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15
Q

T-type VDCC Inhibitor

A

Verapamil

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16
Q

Chronotropic effect

A

Effect on the Heart Rate

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17
Q

Dromotropic effect

A

Effect on the Speed of conduction

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18
Q

Role of Gβγ in M2-R

A

Activation of GIRK channels

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19
Q

Sympathetic heart regulation

A
  • NE on B1-AR
  • Gs, more cAMP
    Threshold is reached faster with (I)f, so faster AP rate
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20
Q

Parasympathetic heart regulation

A
  • Right Vagus: SA
  • Left Vagus: AV
  • Ach on M2-R
  • Gi, less cAMP
  • Gγβ, hyperpol.
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21
Q

Does the Vagus nerve innervate the ventricles in Humans?

A

No

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22
Q

Hormone effects on HR (Epi, and TH)

A
  • Epineph: similar to NE
  • Hyperthyroidism: Tachycardia
  • Hypothyroidism: Bradycardia
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23
Q

B1-R blocker

A

Propranolol
Blocks sympathetic effect

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24
Q

M2-R blocker

A

Atropine
Blocks parasymp. effect
Much stronger effect on parasymp. compared to B1-R blockers

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25
Q

What happens if we use both B1-R and M2-R blockers?

A

Propranolol & Atropine
Produce the intrinsic pacemaker frequency of the SA node
= 100 bpm

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26
Q

SA Node Intrinsic pacemaker freq.

A

100 bpm

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27
Q

AV Node/Bundle of His Intrinsic pacemaker freq.

A

40-60 bmp

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28
Q

Purkinje fibers Intrinsic pacemaker freq.

A

20-40 bpm

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29
Q

Myocytes Intrinsic pacemaker freq.

A

None
Under physiological conditions
(may happen in path.)

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30
Q

What affects conduction velocity?

A
  • Size of current: higher current = faster conduction
  • Resistance: Low R in gap junctions, thicker branches conduct faster
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31
Q

Why does AV node have slowest conduction?

A

Very thin fibers, slower cond.
To delay ventricular contraction

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32
Q

Effective / Absolute refractory period

A

Unresponsive after activation due to inactivated ion channels

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33
Q

Relative refractory period

A

Additional stimulus produces another AP, but needs stronger stimulus

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34
Q

ECG Depolarization and Inflection

A
  • Positive direction= Positive inflection
  • Negative direction= Negative inflection
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35
Q

ECG Repolarization and Inflection

A
  • Positive direction= Negative inflection
  • Negative direction= Positive inflection
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36
Q

Segment vs Interval on ECG

A
  • Segment: Between waves where line is isoelectric
  • Interval: Includes waves
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37
Q

PR (PQ) interval

A
  • Conduction from atria to ventricles
  • 0.12 - 0.20 s
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38
Q

QRS interval

A
  • Ventricular depol.
  • 0.06 - 0.1 s
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39
Q

QT interval

A
  • Ventricular depol. and repol.
  • 0.36 s
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40
Q

Unipolar lead

A

Measures the electric impulse of a point relative to a reference point

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41
Q

Bipolar lead

A

Measures electrical difference between 2 electrodes
(+ & -)

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42
Q

Augmented limb leads (Goldberger)

A
  • Unipolar lead: active/exploring electrode & indifferent/reference electrode
  • In Eindhoven’s Triangle
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43
Q

Angles of Leads on Hexaxial system

A
  • I: 0°
  • II: 60°
  • III: 120°
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44
Q

3 bipolar leads in Eindhoven Triangle

A
  • AVR: R.Arm -150°
  • AVL: L.Arm -30°
  • AVF: Left leg +90°
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45
Q

1st Heart Sound

A
  • AV valve closure
  • Longer, louder, lower frequency
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46
Q

2nd Heart Sound

A
  • AO valve closure
  • Shorter, weaker, higher pitch
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47
Q

Length of Cardiac cycle

A

0.8 s

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48
Q

Systole time vs electrical

A
  • Time: Bw First and second heart sounds
  • Electrical: Beginning of Q wave till end of T wave
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49
Q

Diastole time vs electrical

A
  • Time: After 2nd heart sound till right before 1st heart sound
  • Electrical: Isoelectric interval after T and right before P
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50
Q

Rules for construction of Cardiac cycle

A
  • Liquid is incompressible
  • Pressure gradient determines flow
  • Valves open with blood flow
  • No back-flow through closed valves
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51
Q

Stroke Volume (SV)

A

Amount of blood transported to Aorta in Systole
EDV - ESV
140 - 60 = 80ml

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52
Q

Ejection Fraction (EF)

A

Fraction of ventricular blood ejected
SV / EDV
0.5 < EF < 0.75

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53
Q

EDV

A

140 ml

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54
Q

ESV

A

60 ml

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55
Q

Atrium pressure

A

4 - 8 mmHg

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56
Q

Ventricle pressure

A

4 - 120 mmHg

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57
Q

Aortic pressure

A

80 - 120 mmHg

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58
Q

Systole duration

A

0.27 s

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59
Q

Diastole duration

A

0.53 s

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60
Q

Incisure/Dicrotic Notch

A

Small rise in pressure during diastole representing closure of AO valve

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61
Q

Cardiac Output (CO)

A

Volume of blood being pumped by L.Ventricle into Aorta / min
= 5.6 L/m (rest)
HR x SV (70 x 80)

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62
Q

Total Peripheral Resistance (TPR)

A

Total resistance that must be overcome to push the blood through the circulatory system and create flow
(P.art. - P.ven.) / CO
1/tpr = 1/Parm + 1/Pleg + 1/Pbrain

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63
Q

Mean arterial B.P

A

93 mmHg
CO x TPR
(Psys * 2xPdia) / 3

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64
Q

Why when calculating MABP we use 2x the Pdiastolic

A

Because since Diastole (0.53s) lasts almost 2x longer than Systole (0.27s), we give it a larger weighing by doing this

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65
Q

Regulation of CO

A
  • Heterometric Reg.
  • Homometric Reg.
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66
Q

Heterometric Regulation

A

How different initial fiber lengths impact contraction force

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67
Q

Otto Frank’s Experiment

A
  • Proves Heterometric regulation.
  • Higher preload, stronger contraction
  • Greater fiber length, more forceful contraction
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68
Q

Starling’s Experiment

A
  • Proves Heterometric regulation.
  • Increased venous return, increasing EDV, led to greater stroke volume
69
Q

Frank-Starling Law

A

Stroke Volume increases in response to increased ventricular blood volume (EDV), when all other factors remain constant

70
Q

Preload

A

Increased venous return and Ventricular filling (EDV)

71
Q

Afterload

A

Aortic pressure against which the heart pumps

72
Q

Effects of increased afterload on BP

A

Systolic and Diastolic pressures both increase, but with a constant difference bw them
Arterial pressure increases

73
Q

Homometric Regulation

A

Force of contraction is changed independently of fiber length

74
Q

Sympathetic Homometric Reg.

A

B1-AR = PKA
1) L-VGCC & RyR act. (Ca release)
2) TnI inhibits Ca binding to tropomyosin, Faster relaxation
3) Phospholamban act, regulates SERCA (in bw beats)

75
Q

What Drug can achieve same results as Sympathetic Homometric Regulation

A

Isoproterenol
(B-AR agonist)

76
Q

Parasympathetic Homometric Reg.

A

M2-AR = Less PKA
1) No phosph. & activation of Ryr, VGCC, TnI
2) GIRKs activated = K+
3) Atria and conducting system effected ONLY

77
Q

Other factors that influence contractility

A
  • Temperature
  • Ion concentrations
  • Hypoxia, Ischemia
78
Q

Vessel ramification

A

Aorta
(10^4) Small Arteries
(10^7) Arterioles
(4x10^10) Capillaries

79
Q

Blood Volume in A, C, V, H

A
  • A: 13%
  • C: 7%
  • V: 64%
  • H: 7%
80
Q

Bernoulli’s Law

A

Increase in speed of slow (dynamic pressure) occurs simultaneously with a decrease in hydrostatic pressure (side pressure)

81
Q

Reynold’s Number

A

Tendency of a flow to be Turbulent or Laminar
<2000 : Laminar
>3000 : Turbulent
= (densDv) / n (visc)

82
Q

Laplace’s Law

A

Tension within the wall of a sphere filled with a particular pressure depends on the thickness of the blood vessel wall

83
Q

What vessels are Veins and Arterioles called?

A
  • Veins: Capacitance vessels
  • Arterioles: Resistance vessels
84
Q

Windkessel Effect

A

Converts intermittent pulsatile flow from heartbeat to steady flow.
In Aorta & Large arteries (elastic)

85
Q

What forms resting/Basal tone of Arterioles

A
  • Myogenic tone (SMC)
  • Sympathetic tone
86
Q

Lung type vessels

A
  • Contain elastic fibers
  • Works under Passive mech.
  • Very Compliant
  • When Diameter increases, Resistance decreases
87
Q

Kidney type vessels

A
  • Contain smooth muscles
  • Work under Active mech.
  • Maintain BF in certain range via autoreg.
  • Pressure increase, Resistance increase (due to tension)
88
Q

Why does resistance increase in Kidney type vessels with larger pressure?

A

1) SMC contains stretch activated non-spec. cation channels
2) Depol. activates VGCC
3) Vasoconstriction (Bayliss)

89
Q

Non-invasive BP measurement

A

Sphygmomanometry
Cuff inflated to P greater that Psys then slowly releases

90
Q

Pulse pressure

A

Psys - Pdia = 120 - 80 = 40 mmHg

91
Q

Effects of Increasing CO

A
  • Overall Pressure increase
  • Psys more affected
  • Ppulse increases
92
Q

Effects of Increasing TPR

A
  • Changes Psys & Pdia equally
  • No change in Ppulse due to equal change
93
Q

Effects of Lower compliance

A
  • Psys Increases
  • Pdia decreases
  • Higher Ppulse
94
Q

1 cmH2O in mmHg

95
Q

Effects of Hormones on TPR

A
  • Estrogen: Vasodilator, lower TPR
  • Testosterone: Vasoconstrictor, higher TPR
96
Q

Mean Pressure in Systemic Vessels
(Aorta, Arteries, Arterioles, Capillaries, Veins)

A

100, 85, 35, 15, 0

97
Q

Mean Pressure in Pulmonary Vessels
(Arteries, Veins)

98
Q

Terminal Arterioles

A
  • Smallest arterioles
  • 10-50 um
  • Highest in number
  • Single layer of SM (symp. inn)
99
Q

Metarterioles

A
  • Smaller than terminal arterioles
  • Discontinuous SM layer (not inn)
  • Origin of Capillaries
  • Material exchange
100
Q

Precapillary Sphincter

A
  • One smooth muscle cell that surrounds the capillary
  • Determines Open/Closed state of capillary
  • Modulation of blood flow
101
Q

True Capillaries

A
  • Smallest vessel
  • Exchange site
  • 5-7 um
  • Only endothelial cells (no SM)
  • Have pores
102
Q

Postcapillary Venules

A
  • Carry blood back to veins
  • Discontinuous SM
  • May exchange across wall
103
Q

ArterioVenous Shunt (AV-shunt)

A
  • Bypass bw Arterial & Venous systems
  • Direct link bw arteriole and venule
  • NOT part of microcirculation
  • Found in skin for thermoregulation (symp. control)
104
Q

Continuous Capillaries
(Tight Capillary)

A
  • Most abundant (muscle, skin, lung)
  • Tight junctions
  • 100-200nm
  • Pinocytotic Vesicles
105
Q

Fenestrated Capillaries

A
  • For huge substance exchange
  • Larger pore diameter
  • Decreased wall thickness
106
Q

Sinusoid (Discontinuous) Capillaries

A
  • Pore is 1um range (even rbcs cells can cross)
  • Liver, spleen, bone marrow
107
Q

3 Types of Diffusion through Capillary wall

A
  • Diffusion (ions)
  • Pinocytosis (large molecules)
  • Hydrodynamic fluid exchange (pores)
108
Q

Capillary Hydrostatic Pressure Art & Venous

A
  • Arteriolar: 30 - 35 mmHg
  • Venous: 10 - 15 mmHg
109
Q

Interstital Hydrostatic Pressure

A

Usually Negative, but 1mmHg in organs with a Capsule

110
Q

Capillary & Interstitial Oncotic pressure (colloid osmotic)

A
  • C: 25 mmHg
  • I: 5 mmHg
    (Proteins)
111
Q

Total filtration Volume in Microcirculation

A
  • 20 ml/min Filtrated
  • 18 ml/min Absorbed
  • 2 ml/min in interstitium goes to Lymph
112
Q

Vasomotion

A

Vascular SM in periphery undergo cyclic contraction and relaxation to improve flow

113
Q

Local vs Systematic Arteriolar resistance

A
  • Local: P = Q * R
  • Systematic: P = CO & TPR
114
Q

How does cAMP relate to muscle contraction

A

1) Adenlyly Cyclase makes cAMP
2) cAMP activates PKA
3) PKA phosphorylates & inh. MLCK
4) No phosphorylation of Myosin LC
5) No contraction

115
Q

How does cGMP relate to muscle contraction

A

1) Guanylyl Cyclase makes cGMP
2) cGMP activates PKG
3) PKG inh. IP3-R
4) PKG act. MLCP
5) K+ channel opening

116
Q

Physiological Vasoconstrictors

A
  • NE (a1-AR)
  • Angiotensin II
  • Endothelin I
  • TXA2
  • ADH / Vasopressin
117
Q

Physiological Vasodilators

A
  • Adenosine
  • PGE2
  • PGI2
  • NO
  • ANP (cGMP)
118
Q

Starling Forces

A

Forces that control movement of Fluid in and out of Capillaries
(Hydrostatic and Oncotic Pressures)

119
Q

Effective Filtration Pressure

A
  • Positive: Filtration
  • Negative: Absorption
    θ = Reflection coefficient describes how permeable membrane is. (0=H2O, 1= Albumin)
120
Q

What makes up Lymphatic System

A
  • Lymphatic Capillaries
  • Collecting Lymphatics
  • Lymph Node
  • Central Lymphatics
121
Q

Lymphatic Capillaries

A
  • Blind ended
  • Uptake of fluid & Large molecules
  • Button-like junctions functioning as primary valves to stop back-flow to interstitial valves
122
Q

Collecting Lymphatics

A
  • Zipper like junctions
  • Lymphatic valves
  • SMC coverage
  • Maintains forward flow
123
Q

Lymph Node

A
  • Efferent/Afferent Lymph vessels
  • Sampling and filtering in peripheral structures
124
Q

Central Lymphatics

A
  • Thoracic/Right lymphatic Duct
  • Lymphovenous valve separates blood and Lymph components
125
Q

Interstital Fluid makeup

A
  • Gel Phase (99%): Hydrate coat of matrix proteins, PG, GAG, Hy. acid
  • Soluble Phase (1%): Free fluid
126
Q

What factor induce Lymphatic growth in Development?

A

VEGFC
Vasculoendothelial GF C

127
Q

Central Venous Pressure (CVP)

A

0 - 2 mmHg
Pressure of Vena Cava and Right Atrium

128
Q

Mean systemic filling pressure (MSFP)

A

Average pressure in Veins and Arteries when heart isnt pumping
= 7 mmHg in Cardiac arrest

129
Q

Factors influencing Venous P changes

A
  • Retrograde effect of Heart function
  • Respiration
  • Foot veins (Skeletal M)
  • Walking
130
Q

Pump functions on Venous system

A
  • Peripheral musculovenous Pump
  • Thoraco-abdominal Pump
131
Q

Fast-acting Baroreceptors
(High P B.C)

A
  • Stretch receptors in Aortic arch and carotid sinuses
  • Sensitive in range 50-200 mmHg (carotid), 100-200 mmHg (aortic)
  • Contain Elastic fibers
132
Q

Slow-acting Baroreceptors
(High P B.C)

A
  • Renin-Angiotensin system
  • Detects P drop in Renal A. via mechanoreceptors in afferent arterioles of Kidney
  • Pressure drop = Renin secretion
  • Leads to ANGII (vasoconstrictor)
133
Q

Low-Pressure Baroceptors

A
  • Found within Venous system
  • Sense changes in Blood Volume
  • S/I Vena Cava & RA sinus venarum cavarum
  • Help by Na+ excretion
134
Q

Brainbridge Reflex

A
  • Increase in Atrial pressure stimulates baroreceptors that travel via Vagus N to NTS to Increase HR
  • Leads to more CO and increased GFR in kidney
135
Q

Peripheral Chemoreceptors

A
  • Near bifurcation of Common carotid and Aortic arch
  • pO2 sensitive (mostly)
136
Q

Central Chemoreceptors

A
  • In Medulla behind BBB
  • pCO2 sensitive
137
Q

Cushing Reflex

A

Increased intracranial pressure compresses cerebral arteries and activates Central chemoreceptors and CVLM lowers HR
BP still high cause no communication bw CVLM & RVLM

138
Q

What carries Baroreceptor Information to Brain centers?

A
  • Aortic: Vagus Nerve
  • Carotid: Glossopharyngeal N
    (both to NTS in Medulla)
139
Q

What happens when NTS is stimulated

A

Depressor effect

140
Q

Cardiopulmonary Baroreceptor

A
  • Low-pressure Baroreceptor
  • Type A: Tension during atrial Systole
  • Type B: Tension during atrial Diastole
    (Info to Vagal center)
141
Q

Respiratory sinus arrhythmia

A
  • Inhalation causes Sympathetic stimulation
  • Exhalation causes Parasympathetic stimulation
    Affected mostly by Vagal stimulation since ACh acts quicker
142
Q

Chemoreceptor Reflex

A
  • Primary effect: Medullary Vagal center slows down HR to reduce O2 usage (hypercapnia)
  • Secondary effect: Inhibits medullary vagal center, increased HR (hypocapnia)
143
Q

Local Hypoxia

A

1) Low intracellular ATP
2) ATP-act. K+ channels open
3) Hyperpolarization
4) L-VGCC decrease act
5) Vasodilation

144
Q

Reactive Hyperemia /Hypoxia

A

Increase in perfusion due to a short period of Ischemia
- Increase in BF is proportional to length of Ischemia

145
Q

PGI2 effects

A

Can cause vasodilation by increasing cAMP through Gs coupled-R

146
Q

AVDO2 Arterial

147
Q

AVDO2 Venous

148
Q

AVDO2 Body Average

149
Q

AVDO2 Heart

A

120 - 130 ml/L

150
Q

pO2

151
Q

pCO2

152
Q

Flow to Heart Rest/Exercise

A
  • Rest: 250 ml/min
  • Exercise: 1250 ml/min
153
Q

O2 consumption of Heart

154
Q

Transmural Pressure in heart

A

= Extramural - Intramural P
- Ex.M: Ventricle P
- Intra. M: Aortic P

155
Q

Blood flow to Skeletal Muscle Rest/Exercise

A
  • Rest: 800 - 1000 ml/min
  • Exercise: 20x higher
156
Q

AVDO2 Skeletal Muscle

157
Q

Flow to Splanchnic and O2 consumption

A

1000 - 1500 ml/min
Uses 40 ml/min

158
Q

AVDO2 Splanchnic

159
Q

What can Cholecystokinin and Gastrin cause in Splanchnic circulation

A

Vasodilation

160
Q

Sympathetic effect on Splanchnic Circulation

A

Venoconstriction
(a1-AR)
Increased venous return and CO

161
Q

Flow Cutaneous Circulation

A

100 - 300 ml/min

162
Q

AVDO2 Cutaneous

A

20 - 30 ml/L

163
Q

Where does Thermoregulation happen

A

Apical Skin (Palms, Face, Plantar)
- Arteriovenous anastomosis

164
Q

AVDO2 Brain

165
Q

Flow of Brain and O2 consumption

A

850 ml/min
Consumes 30 ml/L

166
Q

Main Blood supply of Brain

A
  • ICA: 350 ml/min
  • Vertebral A: 75 ml/min
167
Q

Perfusion P in brain when standing

A

15 mmHg less than MABP
93 - 15
= 78 mmHg

168
Q

Total CSF

169
Q

Daily CSF production

A

500 ml/day
and is equal to absorption cause amount is always constant

Physiology 1 (12 decks)

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