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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
Q

Conduction of Cardiac AP

A

Not the same in all myocardial tissues

  • slowest in AV node (adequate filling)
  • fastest in His/Purkinje to ensure quick activation of ventricles
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26
Q

Modulation of Pacemaker Activity

A

Cardiac slow response cells

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27
Q

Changes in Pacemaker Activity

A 
Emotions
Blood pressure
Drugs
Hormones
Etc
  • change rate of depolarization of phase 4 (change gK, gNa, gCa)
  • change threshold potential
  • change maximal diastolic potential
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28
Q

ANS Impact on SA node: Acetylcholine

A

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)

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29
Q

ANS Impact on SA Node: Norepinephrine

A

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
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30
Q

Chronotropic Effects

A

Effects of ANS on heart rate

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31
Q

Dromotropic Effects

A

Effects of ANS on conduction velocity

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32
Q

Inotropic Effects

A

Effects of ANS on contractility

Pos –> greater force of contraction of ventricles –> more blood out

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33
Q

Electrocardiogram

A

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

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34
Q

Recording the EKG

A

Electrodes on surface of body

Pos wave of depolarization advances toward pos electrode, upward deflection recorded on EKG

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35
Q

Active (exploring) Electrode

A

Senses the electrical field

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36
Q

Passive (indifferent) Electrode

A

Reference electrode (not sensing the field - almost like a ground)

Considered to be at 0mV

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37
Q

Lead

A

Combination of 2 electrodes

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38
Q

Unipolar Lead

A

Active plus passive electrode

Measure the voltage only at active electrode

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39
Q

Bipolar Lead

A

Two active electrodes

Measure the voltage difference bt the two electrodes

40
Q

Standard Limb Leads

A

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
Q

Augmented Limb Leads

A

Unipolar leads

aVR, aVL, aVF

Bisecting corners of Einthoven’s triangle

42
Q

Frontal and Horizontal Plane Leads

A

Chest leads (6)

SLIDE 28

43
Q

10 electrodes on patient …

A

12 leads!

Standard: I, II, III
Augmented: aVR, aVL, aVF
Precordial: V1-V6

44
Q

ECG Intervals and Waves

A 
P wave
QRS complex
ST segment
T wave 
U wave (sometimes)

PR
QT

45
Q

P Wave

A

Atrial depolarization

46
Q

QRS Complex

A

Ventricular depolarization

47
Q

T Wave

A

Ventricular repolarization

Upright wave form - repolarize backwards - outside (epi) to inside (endo)

48
Q

Normal Sinus Rhythm

A

Rate: 60-100 bpm

Rhythm originates at SA node and reflects normal electrical activity

49
Q

Measure Heart Rate

A

P-P interval = atrial rate

R-R interval = ventricular rate

50
Q

Sympathetic Activation

A

Increased heart rate
-shorten P-P, R-R intervals

Increased conduction through AV node
-dec P-R interval (inc speed)

51
Q

Parasympathetic Activation

A

Decreased heart rate
-inc P-P, R-R interbals

Decreased conduction through AV node
-inc P-R interval

No vagal innervation of ventricles

52
Q

Atrial excitation and contraction should be …

A

completed before the onset of ventricular contraction

Ensures complete ventricular filling

53
Q

Excitation of cardiac muscle should be …

A

coordinated to ensure that each heart chamber contracts as a unit

Ensures efficient pumping

54
Q

The pair of atria and ventricles should be …

A

functionally coordinated so that both members of the pair contract simultaneously

55
Q

Cardiac Muscle Contraction (steps)

A

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
Q

Tension

A

Proportional to ICF Ca concentration

More Ca –> greater tension

57
Q

Skeletal Muscle

A

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
Q

Cardiac Muscle

A

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
Q

The Cardiac Cycle

A

Diastole + Systole

The mechanical and electrical events that define one phase of cardiac filling and emptying

Duration=60(s/min)/HR

60
Q

Diastole

A

Ventricular relaxation and filling

Perfusion of coronary arteries

61
Q

Systole

A

Ventricular contraction and ejection

62
Q

Phases of Cardiac Cycle

A 
Atrial systole (D)
Isovolumic contraction (S)
Rapid ejection (S)
Reduced ejection (S)
Isovolumic relaxation (D)
Rapid filling (D)
Reduced filling (D)
63
Q

Atrial Systole

A

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
Q

Isovolumic Ventricular Contraction

A

Marks beginning of QRS complex

First heart sound heard (S1) - closure of AV valves close

65
Q

Rapid Ventricular Ejection

A

Most of stroke volume ejected now –> dec in ventricular volume

66
Q

Reduced Ventricular Ejection

A

T wave begins (starts to repolarize)

67
Q

Isovolumic Ventricular Relaxation

A

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
Q

Rapid Ventricular Filling

A

Mitral valve opens as ventricular pressure falls below atrial pressure

LV filling begins

69
Q

Reduced Ventricular Filling

A

Diastasis

Longest phase, final ventricular filling

P wave begins during this phase

70
Q

Pressure Volume Loop

A

Plot of pressure v. volume for one cardiac cycle

Counterclockwise direction

71
Q

LAP

A

Left atrial pressure

Pressure at which mitral valve opens

72
Q

EDP

A

End diastolic pressure

End of diastole

73
Q

DBP

A

Diastolic blood pressure

Right before ejection

Lowest ARTERIAL pressure of cardiac cycle

74
Q

SBP

A

Systolic blood pressure

Greatest pressure in AORTA

75
Q

Stroke Volume (SV)

A

Volume of blood ejected from one ventricular contraction each time the heart beats

SV=EDV-ESV

Normal: 75 ml/beat

76
Q

Cardiac Output (CO)

A

Amount of blood pumped by the heart each minute

CO=SV x HR

Normal: 5 L/min

77
Q

Ejection Fraction (EF)

A

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
Q

Increasing Muscle Length

A

Inc Ca sensitivity of troponin (more myosin exposed)

Inc Ca release from SR

79
Q

Length Tension Relationship

A

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
Q

Preload

A

The resting length from which the muscle contracts

Bigger preload - bigger contraction

81
Q

Length:tension

A

Volume:pressure

As volume increases, ventricular pressure increases

82
Q

Length-Tension Relationship

A

Inc preload –> inc sarcomere length toward optimum actin myosin overlap

83
Q

Left Ventricular End Diastolic Volume

A

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
Q

Afterload

A

The force against which cardiac muscle shortens

The load on the muscle during contraction

LV: afterload = aortic pressure

85
Q

Hypertension

A

Increased afterload - harder to get SV out

86
Q

Hypotension

A

Decreased afterload - easier to get blood out

87
Q

Acute Increased Afterload

A

= dec SV

blood remaining inc preload = restore SV

88
Q

Chronic Increased Afterload

A

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
Q

Contractility

A

Change in performance at a given preload

Changes due to intracellular dynamics of Ca

  • inc contractility = more Ca
  • dec contractility = less Ca
90
Q

Volume ejected in systole is determined by

A

EDV

91
Q

Positive Inotropic Effect

A

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
Q

Negative Inotropic Effect

A

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
Q

Factors determining overall force of ventricular contraction

A

Preload

Contractility

SLIDE 50

94
Q

Frank Starling Relationship

A

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
Q

Frank

A

P developed during systole in a ventricle and the vol present in ventricle just prior to systole

96
Q

Starling

A

vol the ventricle ejected in systole was determined by EDV

PHA 511 (7 decks)

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