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PHA 511 > 5. Cardiac Physiology I > Flashcards

5. Cardiac Physiology I Flashcards

1
Q

Cardiovascular System (function)

A

Pump blood

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2
Q

Cardiovascular System

A 
Closed circuit
2 sides (pulmonary, systemic)
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3
Q

Ventricular Contraction

A

Ventricles must be activated to contract

Electrical activation from cardiac action potentials

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4
Q

Venous Return

A

VR

Rate at which blood is returned to the heart

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5
Q

Cardiac Output

A

CO

Rate at which blood is pumped from ventricles

Total systemic blood flow

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6
Q

CO and VR

A

In a steady state, VR=CO

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7
Q

Right Heart

A

Pulmonary

100% of blood from R ventricle goes to lungs and gets oxygenated

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8
Q

Left Heart

A

Systemic

100% of ventricular output goes out to body

Distribution varies - different % to different body systems/parts - all adds up to 100%

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9
Q

Conduction Pathway of the Heart

A
  1. Cardiac AP originates at SA node (pacemaker)
  2. Distributed out through internodal tracts to R and L atria
  3. AV node - conduction slows down to ensure adequate ventricular filling
  4. Bundle of His
  5. R and L bundle branch
  6. Last point of depolarization, L ventricle
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10
Q

SA Node

A

Pacemaker of the heart

Spontaneously depolarizes

Sets tone of heart rate

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11
Q

Action Potentials from Various Cardiac Cells Differ

A

Fast response (contractile) v. slow response (pacemaker/conducting)

Slide 8

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12
Q

Pacemaker Cell

A

Slow response

Display automaticity

  • do NOT require CNS input to elicit AP (can be modified by CNS)
  • unstable RMP –> rhythmic APs

gNa is greater
gCa is greater
gK is lower than in fast response cells

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13
Q

Cardiac APs: Phase 4

A

Spontaneous depolarization or pacemaker potential

Longest portion of SA nodal AP

Accounts for automaticity of SA cells

MDP occurs

Slow depolarization (opening of Na channels = funny current (If) = causes rise in MP)

Rate of rise sets heart rate

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14
Q

MDP

A

Maximum diastolic potential

Point of maximum repolarization

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15
Q

Cardiac APs: Phase 0 (slow response)

A

Upstroke

Increased gCa via L type channels
(also some T type)

Overshoot potential less positive than fast response (above 0 for a bit)

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16
Q

Cardiac APs: Phase 3 (slow response)

A

No phase 1 or 2

Cellular repolarization

  • inc K (outward) current
  • inactivation of Ca current

Similar to fast response

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17
Q

Non-Pacemaker

A

Fast response

Occur in atria, ventricles, purkinje fibers

Rapid repolarization

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18
Q

Gap Junctions

A

Found in intercalated disks

Low resistance pathways

  • functional syncytium
  • directly transmits depolarizing current across the entire heart

Instantaneous, bidirectional - allows functioning as unit

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19
Q

Non-Pacemaker Cardiac APs: Phase 0

A

Resting membrane potential: -90mv
-gK&raquo_space;gNa

Due to large, transient inc in gNa (-70 mV)

Initial stimulus: Na and Ca movement into cell via gap junctions

Threshold around -70mV

Na and Ca movement from SA nodal cells

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20
Q

Non-Pacemaker Cardiac APs: Phase 1

A

Decrease gNa (inactivation)

Increase gK (transient outward current - inactivates very quickly)

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21
Q

Non-Pacemaker Cardiac APs: Phase 2

A

Plateau due to gradual inc in gCa via L type Ca channels (began to open at -35 to -10 mV)

Balanced by dec in normally high resting gK

Holding membrane in depolarized state

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22
Q

Non-Pacemaker Cardiac APs: Phase 3 and 4

A

Full repolarization due to inc in gK

IRK voltage activation of gNa, gCa

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23
Q

Normal Heart Rate

A 
60-100 = normal
50-70 = ideal
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24
Q

Latent Pacemakers

A

Cells in other areas of heart have capacity for spontaneous phase 4 depolarization

Intrinsic automaticity

Cells with the fastest rate of phase 4 depolarization control the heart rate

SA node (60-100) –> atrial foci (60-80) –> AV node (40-60) –> ventricular foci (20-40)

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25
Conduction of Cardiac AP
Not the same in all myocardial tissues - slowest in AV node (adequate filling) - fastest in His/Purkinje to ensure quick activation of ventricles
26
Modulation of Pacemaker Activity
Cardiac slow response cells
27
Changes in Pacemaker Activity
``` Emotions Blood pressure Drugs Hormones Etc ``` - change rate of depolarization of phase 4 (change gK, gNa, gCa) - change threshold potential - change maximal diastolic potential
28
ANS Impact on SA node: Acetylcholine
Parasympathetic Muscarinic receptors Dec slope of phase 4 (shifted R and down) ``` Inc gK (hyperpolarize) Dec gCa ``` MDP dropped more negative (further from threshold - longer to get to threshold - slows down HR)
29
ANS Impact on SA Node: Norepinephrine
Sympathetic Beta 1 receptors Inc slope of phase 4 (inc gNa and gCa (T type channels)) Accelerates phase 3 repolarization - shortens AP duration - inc discharge frequency
30
Chronotropic Effects
Effects of ANS on heart rate
31
Dromotropic Effects
Effects of ANS on conduction velocity
32
Inotropic Effects
Effects of ANS on contractility Pos --> greater force of contraction of ventricles --> more blood out
33
Electrocardiogram
Surface recording of the entire heart Based on conductile system (APs traveling through the heart activating muscle to contract) NOTE THE RELATION OF AP CONDUCTION TO ECG
34
Recording the EKG
Electrodes on surface of body Pos wave of depolarization advances toward pos electrode, upward deflection recorded on EKG
35
Active (exploring) Electrode
Senses the electrical field
36
Passive (indifferent) Electrode
Reference electrode (not sensing the field - almost like a ground) Considered to be at 0mV
37
Lead
Combination of 2 electrodes
38
Unipolar Lead
Active plus passive electrode Measure the voltage only at active electrode
39
Bipolar Lead
Two active electrodes Measure the voltage difference bt the two electrodes
40
Standard Limb Leads
Bipolar limb leads 3 bipolar leads make up Einthoven's Triangle - heart in center Lead 1: RA -, LA + Lead 2: RA -, LL + Lead 3: LA -, LL + Lead 2: in line with normal conduction system of heart
41
Augmented Limb Leads
Unipolar leads aVR, aVL, aVF Bisecting corners of Einthoven's triangle
42
Frontal and Horizontal Plane Leads
Chest leads (6) SLIDE 28
43
10 electrodes on patient ...
12 leads! Standard: I, II, III Augmented: aVR, aVL, aVF Precordial: V1-V6
44
ECG Intervals and Waves
``` P wave QRS complex ST segment T wave U wave (sometimes) ``` PR QT
45
P Wave
Atrial depolarization
46
QRS Complex
Ventricular depolarization
47
T Wave
Ventricular repolarization Upright wave form - repolarize backwards - outside (epi) to inside (endo)
48
Normal Sinus Rhythm
Rate: 60-100 bpm Rhythm originates at SA node and reflects normal electrical activity
49
Measure Heart Rate
P-P interval = atrial rate | R-R interval = ventricular rate
50
Sympathetic Activation
Increased heart rate -shorten P-P, R-R intervals Increased conduction through AV node -dec P-R interval (inc speed)
51
Parasympathetic Activation
Decreased heart rate -inc P-P, R-R interbals Decreased conduction through AV node -inc P-R interval No vagal innervation of ventricles
52
Atrial excitation and contraction should be ...
completed before the onset of ventricular contraction Ensures complete ventricular filling
53
Excitation of cardiac muscle should be ...
coordinated to ensure that each heart chamber contracts as a unit Ensures efficient pumping
54
The pair of atria and ventricles should be ...
functionally coordinated so that both members of the pair contract simultaneously
55
Cardiac Muscle Contraction (steps)
Contractile or autorhythmic cell connected to contractile cell by gap junctions 1. Current spreads through gap junctions to contractile cell 2. AP travel along plasma membrane and T tubules 3. Ca channels open in plasma membrane (external) and SR (internal) 4. Ca induces Ca release from SR 5. Ca binds to troponin, exposing myosin binding sites 6. Crossbridge cycle begins (muscle fiber contracts) 7. Ca is actively transported back into SR and ECF 8. Tropomyosin blocks myosin binding sites (muscle fiber relaxes)
56
Tension
Proportional to ICF Ca concentration More Ca --> greater tension
57
Skeletal Muscle
Voluntary Striated Multinucleated Non-branching Ca from SR Cannot contract w/out nerve stimulation Muscle fiber stimulated independently (no gap junctions) Nerve Neuromuscular junction Muscle cell
58
Cardiac Muscle
Involuntary Striated Single nucleus Branching Ca from SR, ECF Can contract w/out nerve stimulation - AP originate in pacemaker cells Gap junctions present as intercalated discs Autorhythmic cells Gap junctions Contractile cell
59
The Cardiac Cycle
Diastole + Systole The mechanical and electrical events that define one phase of cardiac filling and emptying Duration=60(s/min)/HR
60
Diastole
Ventricular relaxation and filling | Perfusion of coronary arteries
61
Systole
Ventricular contraction and ejection
62
Phases of Cardiac Cycle
``` Atrial systole (D) Isovolumic contraction (S) Rapid ejection (S) Reduced ejection (S) Isovolumic relaxation (D) Rapid filling (D) Reduced filling (D) ```
63
Atrial Systole
Preceded by P wave At the end of this phase, the vol of blood in LV is maximal (EDV ~120) During diastole Atrial muscle contracting to fill ventricles
64
Isovolumic Ventricular Contraction
Marks beginning of QRS complex First heart sound heard (S1) - closure of AV valves close
65
Rapid Ventricular Ejection
Most of stroke volume ejected now --> dec in ventricular volume
66
Reduced Ventricular Ejection
T wave begins (starts to repolarize)
67
Isovolumic Ventricular Relaxation
Begins after ventricles are fully repolarized (end of T wave) Aortic valve closes slightly before pulmonic valve creating S2 Ventricular blood volume is now at lowest point Volume remaining = ESV (~50)
68
Rapid Ventricular Filling
Mitral valve opens as ventricular pressure falls below atrial pressure LV filling begins
69
Reduced Ventricular Filling
Diastasis Longest phase, final ventricular filling P wave begins during this phase
70
Pressure Volume Loop
Plot of pressure v. volume for one cardiac cycle Counterclockwise direction
71
LAP
Left atrial pressure | Pressure at which mitral valve opens
72
EDP
End diastolic pressure End of diastole
73
DBP
Diastolic blood pressure Right before ejection Lowest ARTERIAL pressure of cardiac cycle
74
SBP
Systolic blood pressure Greatest pressure in AORTA
75
Stroke Volume (SV)
Volume of blood ejected from one ventricular contraction each time the heart beats SV=EDV-ESV Normal: 75 ml/beat
76
Cardiac Output (CO)
Amount of blood pumped by the heart each minute CO=SV x HR Normal: 5 L/min
77
Ejection Fraction (EF)
Fraction of EDV ejected with one SV Effectiveness of ventricles in ejecting blood Indicator of contractility EF=SV/EDV x 100% Normal: 55-75% ``` Dec = problematic Inc = no problems ```
78
Increasing Muscle Length
Inc Ca sensitivity of troponin (more myosin exposed) Inc Ca release from SR
79
Length Tension Relationship
The length of a single L ventricular muscle fiber just prior to contraction corresponds to L ventricular end diastolic volume The tension of a single L ventricular muscle fiber corresponds to the tension/pressure developed by the entire L ventricle
80
Preload
The resting length from which the muscle contracts Bigger preload - bigger contraction
81
Length:tension
Volume:pressure As volume increases, ventricular pressure increases
82
Length-Tension Relationship
Inc preload --> inc sarcomere length toward optimum actin myosin overlap
83
Left Ventricular End Diastolic Volume
aka end diastolic fiber length preload for the L ventricle Greater EDV - greater stretch on ventricles - greater force of contraction to get out of SV to get out EF
84
Afterload
The force against which cardiac muscle shortens The load on the muscle during contraction LV: afterload = aortic pressure
85
Hypertension
Increased afterload - harder to get SV out
86
Hypotension
Decreased afterload - easier to get blood out
87
Acute Increased Afterload
= dec SV blood remaining inc preload = restore SV
88
Chronic Increased Afterload
aka chronic hypertension hypertrophy (lay down more sarcomeres in parallel) Hypertrophy increases the force of contraction at a given preload and helps maintain SV
89
Contractility
Change in performance at a given preload Changes due to intracellular dynamics of Ca - inc contractility = more Ca - dec contractility = less Ca
90
Volume ejected in systole is determined by
EDV
91
Positive Inotropic Effect
Increase in contractility (ie: inc in SV and CO) for a given EDV - dopamine, dobutamine, digoxin, amiodarone - drugs provide more Ca and at a faster rate to the contractile machinery
92
Negative Inotropic Effect
Decrease in contractility (ie: dec in SV and CO) for a given EDV - beta blockers, Ca channel blockers - drugs provide less Ca and at a slower rate to the contractile machinery
93
Factors determining overall force of ventricular contraction
Preload Contractility SLIDE 50
94
Frank Starling Relationship
volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole - ensures that the volume the heart ejects in systole equals the volume it receives in venous return --> closed system - CO at 100% should equal venous return at 100% inc VR --> inc EDV --> bc length tension relationship --> inc SV
95
Frank
P developed during systole in a ventricle and the vol present in ventricle just prior to systole
96
Starling
vol the ventricle ejected in systole was determined by EDV

PHA 511 (7 decks)

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