Heart (2) Flashcards

(169 cards)

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 (Na+)
1) Partial repolarization (K+)
2) Plateau (Ca2+)
3) Complete Repolarization (GIRK)
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 (-80 vs -60/65)
  • 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 (high selectivity)
  • 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
  • Used to lower HR
    (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

GABA-B receptor
Activation of GIRK channels

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19
Q

Sympathetic heart regulation

A
  • NE on B1-AR
  • Gs, more cAMP
  • cAMP activates HCN channels
    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, HCN closed
  • Gγβ, GIRKs open, 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. & 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
What happens if we use both B1-R and M2-R blockers?
Propranolol & Atropine Produce the intrinsic pacemaker frequency of the SA node = 100 bpm
26
Intrinsic pacemaker freq. (SA / AV & His / Purkinje)
- SA: 100 bpm - AV & bundle of His: 40 - 60 bpm - Purkinje: 20 - 40 bpm
27
Myocytes Intrinsic pacemaker freq.
None Under physiological conditions (may happen in path.)
28
What affects conduction velocity?
- Size of current: higher current = faster conduction - Resistance: Low R in gap junctions, thicker branches conduct faster
29
Why does AV node have slowest conduction?
Very thin fibers, slower cond. To delay ventricular contraction
30
Effective / Absolute refractory period
Unresponsive after activation due to inactivated ion channels
31
Relative refractory period
Additional stimulus produces another AP, but needs stronger stimulus
32
ECG Depolarization and Inflection
- Positive direction= Positive inflection - Negative direction= Negative inflection
33
ECG Repolarization and Inflection
- Positive direction= Negative inflection - Negative direction= Positive inflection
34
Segment vs Interval on ECG
- Segment: Between waves where line is isoelectric - Interval: Includes waves
35
PR (PQ) interval
- Conduction from atria to ventricles - 0.12 - 0.20 s
36
QRS interval
- Ventricular depol. - 0.06 - 0.1 s
37
QT interval
- Ventricular depol. and repol. - 0.36 s
38
Unipolar lead
Measures the electric impulse of a point relative to a reference point
39
Bipolar lead
Measures electrical difference between 2 electrodes (+ & -)
40
Augmented limb leads (Goldberger)
- Unipolar lead: active/exploring electrode & indifferent/reference electrode - In Eindhoven's Triangle
41
Angles of Leads on Hexaxial system
- I: 0° - II: 60° - III: 120°
42
3 bipolar leads in Eindhoven Triangle
- AVR: R.Arm -150° - AVL: L.Arm -30° - AVF: Left leg +90°
43
Respiratory Sinus Arrhythmia (pressure-based)
Explains inconsistency of R-R distances in healthy individuals - Inspiration: intrathoracic P & arterial P drop, Baroreceptors not activated, Vagal tone drops, HR increased - Expriation: Opposite, Baroreceptors activated, more Vagal tone
44
1st Heart Sound
- AV valve closure - Longer, louder, lower frequency
45
2nd Heart Sound
- AO valve closure - Shorter, weaker, higher pitch
46
Length of Cardiac cycle
0.8 s
47
Systole time vs electrical
- Time: Bw First and second heart sounds - Electrical: Beginning of Q wave till end of T wave
48
Diastole time vs electrical
- Time: After 2nd heart sound till right before 1st heart sound - Electrical: Isoelectric interval after T and right before P
49
Rules for construction of Cardiac cycle
- Liquid is incompressible - Pressure gradient determines flow - Valves open with blood flow - No back-flow through closed valves
50
Stroke Volume (SV)
Amount of blood transported to Aorta in Systole EDV - ESV 140 - 60 = 80ml
51
Ejection Fraction (EF)
Fraction of ventricular blood ejected SV / EDV 0.5 < EF < 0.75
52
Atrium pressure
4 - 8 mmHg
53
Ventricle pressure
4 - 120 mmHg
54
Aortic pressure
80 - 120 mmHg
55
Systole & Diastole duration
- S: 0.27s - D: 0.53s = 0.8s
56
Incisure/Dicrotic Notch
Small rise in pressure during diastole representing closure of AO valve
57
Cardiac Output (CO)
Volume of blood being pumped by L.Ventricle into Aorta / min = 5.6 L/m (rest) HR x SV = 70 x 80
58
Total Peripheral Resistance (TPR)
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
59
Mean arterial B.P
93 mmHg CO x TPR or (Psys * 2xPdia) / 3
60
Why when calculating MABP we use 2x the Pdiastolic
Because since Diastole (0.53s) lasts almost 2x longer than Systole (0.27s), we give it a larger weighing by doing this
61
Regulation of CO
- Heterometric Reg. - Homometric Reg.
62
Heterometric Regulation
How different initial fiber lengths impact contraction force
63
Otto Frank's Experiment
- Proves Heterometric regulation. - Higher preload, stronger contraction - Due to greater fiber length, so more forceful contraction
64
Starling's Experiment
- Proves Heterometric regulation. - Increased venous return, increasing EDV, led to greater stroke volume
65
Frank-Starling Law
Stroke Volume increases in response to increased ventricular blood volume (EDV), when all other factors remain constant
66
Preload
Increased venous return and Ventricular filling (EDV)
67
Afterload
Aortic pressure against which the heart pumps
68
Effects of increased afterload on BP
Systolic and Diastolic pressures both increase, but with a constant difference bw them Arterial pressure increases
69
Homometric Regulation
Force of contraction is changed independently of fiber length
70
Sympathetic Homometric Reg.
B1-AR = PKA phosphorylates: 1) L-VGCC & RyR act. (Ca release) 2) TnI inhibits Ca binding to tropomyosin, Faster relaxation 3) Phospholamban act, regulates SERCA (in bw beats), faster relax.
71
What Drug can achieve same results as Sympathetic Homometric Regulation
Isoproterenol (B-AR agonist)
72
Parasympathetic Homometric Reg.
M2-AR = Less PKA 1) No phosph. & activation of Ryr, VGCC, TnI 2) GIRKs activated = K+ 3) Atria and conducting system effected ONLY
73
Other factors that influence contractility
- Temperature - Ion concentrations - Hypoxia, Ischemia
74
Vessel ramification
Aorta (10^4) Small Arteries (10^7) Arterioles (4x10^10) Capillaries
75
Blood Volume in A, C, V, H
- A: 13% - C: 7% - V: 64% - H: 7%
76
Bernoulli's Law
Increase in speed of slow (dynamic pressure) occurs simultaneously with a decrease in hydrostatic pressure (side pressure) - When flow speed increases, side pressure decreases
77
Hagen-Poiseuille Law
Largest volumetric flow rate (Iv) is achieved in vessel with largest diameter
78
Reynold's Number
Tendency of a flow to be Turbulent or Laminar <2000 : Laminar >3000 : Turbulent = (dens*D*v) / n (visc)
79
Laplace's Law
Tension within the wall of a sphere filled with a particular pressure depends on the thickness of the blood vessel wall T = (Pxr) / (2xX)
80
What vessels are Veins and Arterioles called?
- Veins: Capacitance vessels - Arterioles: Resistance vessels
81
Windkessel Effect
Converts intermittent pulsatile flow from heartbeat to steady flow. In Aorta & Large arteries (elastic)
82
What forms resting/Basal tone of Arterioles
- Myogenic tone (SMC) - Sympathetic tone
83
Lung type vessels
- Contain elastic fibers - Works under Passive mech. - Very Compliant - When Diameter increases, Resistance decreases
84
Kidney type vessels
- Contain smooth muscles - Work under Active mech. - Maintain BF in certain range via autoreg. - Pressure increase, Resistance increase (due to tension)
85
Why does resistance increase in Kidney type vessels with larger pressure?
1) SMC contains stretch activated non-spec. cation channels 2) Depol. activates VGCC 3) Vasoconstriction (Bayliss)
86
Bayliss Effect
Reflex vasoconstriction of vascular smooth muscle in response to increased vessel pressure/stretch
87
Invasive / Non-invasive BP measurement
- Catheter in Brachial artery: Shows increased Psys, decreases Pdia, larger Ppulse - Sphygmomanometry: Cuff inflated to P greater that Psys then slowly releases
88
Pulse pressure
Psys - Pdia = 120 - 80 = 40 mmHg
89
Effects of Increasing CO
- Overall Pressure increase - Psys more affected - Ppulse increases
90
Effects of Increasing TPR
- Changes Psys & Pdia equally - No change in Ppulse due to equal change
91
Effects of Lower compliance
- Psys Increases - Pdia decreases - Higher Ppulse
92
1 cmH2O in mmHg
0.7 mmHg
93
Effects of Hormones on TPR
- Estrogen: Vasodilator, lower TPR - Testosterone: Vasoconstrictor, higher TPR
94
Mean Pressure in Systemic Vessels (Aorta, Arteries, Arterioles, Capillaries, Veins)
100, 85, 35, 15, 0
95
Mean Pressure in Pulmonary Vessels (Arteries, Veins)
15, 5
96
Terminal Arterioles
- Smallest arterioles - 10-50 μm - Highest in number - Single layer of SM (symp. inn)
97
Metarterioles
- Smaller than terminal arterioles - Discontinuous SM layer (not inn) - Origin of Capillaries - Material exchange
98
Precapillary Sphincter
- One smooth muscle cell that surrounds the capillary - Determines Open/Closed state of capillary - Modulation of blood flow
99
True Capillaries
- Smallest vessel - Exchange site - 5-7 um - Only endothelial cells (no SM) - Have pores
100
Postcapillary Venules
- Carry blood back to veins - Discontinuous SM - May exchange across wall
101
ArterioVenous Shunt (AV-shunt)
- Bypass bw Arterial & Venous systems - Direct link bw arteriole and venule - NOT part of microcirculation - Found in skin for thermoregulation (symp. control)
102
Continuous Capillaries
- Most abundant (muscle, skin, lung) - Tight junctions - 100-200nm wall - Pinocytotic Vesicles
103
Fenestrated Capillaries
- For huge substance exchange - Larger pore diameter - Decreased wall thickness - GI, Endo/Exocrine glands, ...
104
Sinusoid (Discontinuous) Capillaries
- Pore is ~1μm (even RBCs can cross) - Liver, spleen, bone marrow
105
Tight Capillary
- Very strong endothelial connection - No pores - Only highly regulated transcellular transport - Brain (BBB), Retina, ...
106
3 Types of Diffusion through Capillary wall
- Diffusion (ions) - Pinocytosis (large molecules) - Hydrodynamic fluid exchange (pores)
107
Capillary Hydrostatic Pressure Art & Venous
- Arteriolar: 30 - 35 mmHg - Venous: 10 - 15 mmHg
108
Interstital Hydrostatic Pressure
Usually Negative, but 1mmHg in organs with a Capsule
109
Capillary & Interstitial Oncotic pressure (colloid osmotic)
- C: 25 mmHg - I: 5 mmHg (Proteins)
110
Total filtration Volume in Microcirculation
- 20 ml/min Filtrated - 18 ml/min Absorbed - 2 ml/min in interstitium goes to Lymph (~3L/day)
111
Vasomotion
Vascular SM in periphery undergo cyclic contraction and relaxation to improve flow in periphery
112
Local vs Systematic Arteriolar resistance (pressure)
- Local: P = Q * R (ohms) - Systematic: P = CO x TPR
113
How does cAMP relate to muscle contraction
1) Adenlyly Cyclase makes cAMP 2) cAMP activates PKA 3) PKA phosphorylates & inh. MLCK 4) No phosphorylation of Myosin LC 5) No contraction
114
How does cGMP relate to muscle contraction
1) Guanylyl Cyclase makes cGMP 2) cGMP activates PKG 3) PKG inh. IP3-R 4) PKG act. MLCP 5) K+ channel opening
115
Physiological Vasoconstrictors
- NE (a1-AR) = Gq - Angiotensin II - Endothelin I & TXA2 (injured ves.) - Thrombin - ADH / Vasopressin
116
Physiological Vasodilators
- Adenosine - PGE2 - PGI2 - NO (Ca2+ endothelial cells, cGMP) - ANP (cGMP)
117
Starling Forces
Forces that control movement of Fluid in and out of Capillaries (Hydrostatic and Oncotic Pressures)
118
Effective Filtration Pressure & reflection coefficient
- Positive: Filtration (arterial) - Negative: Absorption (venous) θ = Reflection coefficient describes how permeable membrane is. (0=H2O, 1= Albumin)
119
What makes up Lymphatic System
- Lymphatic Capillaries - Collecting Lymphatics - Lymph Node - Central Lymphatics
120
Lymphatic Capillaries
- Blind ended - Uptake of fluid & Large molecules - Button-like junctions functioning as primary valves to stop back-flow to interstitial valves
121
Collecting Lymphatics
- Zipper like junctions - Lymphatic valves - SMC coverage - Maintains forward flow
122
Lymph Node
- Efferent/Afferent Lymph vessels - Sampling and filtering in peripheral structures
123
Central Lymphatics & Outflow
- Thoracic/Right lymphatic Duct - Lymphovenous valve separates blood and Lymph components
124
Interstital Fluid makeup in Tissues
- Gel Phase (99%): Hydrate coat of matrix proteins, PG, GAG, Hy. acid - Soluble Phase (1%): Free fluid
125
What factor induce Lymphatic growth in Development?
VEGFC Vasculoendothelial GF C - Acts on VEGFR3 - Lymphatics develop later than vessels
126
Central Venous Pressure (CVP)
2 - 6 mmHg Pressure of Vena Cava & Right Atrium (0 - 2mmHg) (hydrostatic pressure)
127
Mean systemic filling pressure (MSFP)
Average pressure in Veins and Arteries when heart isnt pumping = 7 mmHg in Cardiac arrest
128
Factors influencing Venous P changes
- Retrograde effect of Heart function - Respiration (pressure) - Leg veins (Skeletal M) - Walking
129
Pump functions on Venous system
- Peripheral musculovenous Pump - Thoraco-abdominal Pump
130
Fast-acting Baroreceptors (High P B.C)
- Stretch receptors in Aortic arch and carotid sinuses - Sensitive in range 50-200 mmHg (carotid), 100-200 mmHg (aortic) - Contain Elastic fibers
131
Slow-acting Baroreceptors (High P B.C)
- Renin-Angiotensin system - Detects P drop in Renal A. via mechanoreceptors in afferent arterioles of Kidney - Pressure drop = Renin secretion - Leads to ANGII (vasoconstrictor)
132
Low-Pressure Baroceptors
- Found within Venous system - Sense changes in Blood Volume - S/I Vena Cava & RA sinus venarum cavarum - Help by Na+ excretion (ANP)
133
Brainbridge Reflex
- 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
134
Peripheral Chemoreceptors
- Near bifurcation of Common carotid and Aortic arch - pO2 sensitive (mostly)
135
Central Chemoreceptors
- In Medulla behind BBB - pCO2 sensitive
136
Cushing Reflex
Life saving reflex in response to low brain perfusion due to high ICP RVLM activates to raise BP, this is sensed by baroreceptors causing Vagal stim of NTS, dropping HR. Brainstem can get compressed so effects breathing. (Hypertension, Bradycardia, Irregular Breathing)
137
What carries Baroreceptor Information to Brain centers?
- Aortic: Vagus Nerve - Carotid: Glossopharyngeal N (both to NTS in Medulla)
138
What happens when NTS is stimulated
Depressor effect (CVLM)
139
Which center RVLM or CVLM has a regulatory function?
CVLM can inhibit RVLM if pressure is too hight
140
Cardiopulmonary (low pressure) Baroreceptors + types
- Low-pressure Baroreceptor - Type A: Tension during atrial Systole - Type B: Tension during atrial Diastole (Info to Vagal center)
141
Respiratory sinus arrhythmia
Lung tissue stretch receptors - Inhalation causes Inh. of Vagal input & more Sympathetic stimulation - Exhalation causes Vagal Parasympathetic stimulation Affected mostly by Vagal stimulation since ACh acts quicker
142
Chemoreceptor Reflex
- Primary effect: Medullary Vagal center slows down HR to reduce O2 usage (for hypercapnia) - Secondary effect: Inhibits medullary vagal center, increased HR to reset balance and supply O2 to Vital organs (for hypocapnia)
143
Local Hypoxia
1) Low intracellular ATP 2) ATP inhibited K+ channels open 3) Hyperpolarization 4) L-VGCC decrease act 5) Vasodilation
144
Reactive Hyperemia /Hypoxia
Increase in perfusion due to a short period of Ischemia - Increase in BF is proportional to length of Ischemia
145
PGI2 effects vessels
- Mainly inhibits platelet adherence to wall or aggregation to prevent clots - Can cause vasodilation by increasing cAMP through Gs coupled receptor
146
Epinephrine on B2-AR
Vasodilation Gs pathway, cAMP, PKA, MLCK inhibition = Relaxation
147
AVDO2 Arterial & Venous & Body average
- A: 200 ml/L - V: 150 ml/L -Body: 50 ml/L
148
AVDO2 Heart & its weight
120 - 130 ml/L 300g
149
Arterial pO2 & pCO2
- pO2: 95 mmHg -pCO2: 40 mmHg
150
Flow to Heart Rest/Exercise
- Rest: 250 ml/min - Exercise: 1250 ml/min
151
O2 consumption of Heart / Body
- Heart: 30 ml/min - Body: 250 ml/min
152
Transmural Pressure in heart
= Extramural - Intramural P - Ex.M: Ventricle P - Intra. M: Aortic P
153
Blood flow to Skeletal Muscle Rest/Exercise
- Rest: 800 - 1000 ml/min - Exercise: 20x higher
154
AVDO2 Skeletal Muscle
60 ml/L (slightly higher than body average)
155
Flow to Splanchnic and O2 consumption
1000 - 1500 ml/min Uses ~40 ml/min (O2)
156
AVDO2 Splanchnic
30 ml/L
157
What hormones cause Vasodilation in Splanchnic
- CCK - Gastrin
158
Sympathetic effect on Splanchnic Circulation
Venoconstriction (a1-AR) Increased venous return and CO
159
Flow Cutaneous Circulation
100 - 300 ml/min
160
AVDO2 Cutaneous
20 - 30 ml/L
161
AVDO2 Brain
60 ml/L
162
Flow of Brain and O2 consumption
850 ml/min Consumes 45 ml/L
163
Main Blood supply of Brain
- ICA: 350 ml/min - Vertebral A: 75 ml/min
164
Perfusion P in brain when standing
15 mmHg less than MABP 93 - 15 = 78 mmHg
165
Can brain sense all ionic changes?
Brain capillaries not permeable to K+ or H+ = Brain tissue not sensitive to Hyperkalemia or Acidosis
166
How can Neuronal activity be sensed
NO levels More active neurons = more NO produced (vasodilation)
167
Total CSF & where does it run
150 ml Subarachnoid Space
168
Daily CSF production
500 ml/day (choroid plex) and is equal to absorption cause amount is always constant
169
CSF vs Plasma
Lower: K+, Ca2+ Negligible cholesterol & Proteins