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Cardiology (SP23) > Module 2: Cardiac Physiology (Weeks 2-3) > Flashcards

Module 2: Cardiac Physiology (Weeks 2-3) Flashcards

1
Q

** FILLER CARD **
Module 2: Video Reviews

A
  • Excitation-contraction coupling
  • The cardiac cycle
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2
Q

** FILLER CARD **

A

C2: Electrophysiology & amp; ECC Slides

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3
Q

Cellular Level
Definitions:
The inside is different (more negative with different concentrations of ions) than the outside

A

Polarized

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4
Q

Cellular Level
What cells in the heart are polarized?

A

Cardiac cells

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5
Q

Cellular Level
How is polarization created?

A

By ions with different concentrations & charges
- This polarization creates a transmembrane potential
- Transmembrane resting potential = -80 to -90 mV

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6
Q

Opening of ion channels is going to result in, what?

A

Depolarization

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7
Q

Returning back to the polarized state is going to result in, what?

A

Repolarization
(back to neg. state)

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8
Q

When there is a trigger within each individual cardiac cell, ion channels open/close creating what?

A

Action Potential

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9
Q

Cardiac Conduction Cells
Definition:
Contractile cells of the atrium & ventricle

A

Cardiomyocytes

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10
Q

Cardiac Conduction Cells
Definition:
Specialized conduction cells

A

Purkinje cells
- Don’t contract but allows current to spread to the heart very quickly

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11
Q

Cardiac Conduction Cells
Definition:
- Sinoatrial (SA or sinus)
- Atrioventricular (AV) node

A

Pacemaker Cells

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12
Q

Action Potentials Types
What do Cardiomyocytes & Purkinje cells use for depolarization (Phase 0)?

A

Na+ channels

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13
Q

Action Potentials Types
What do Automatic (pacemaker) cells use for depolarization (Phase 0)?

A

Slow Ca2+ current

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14
Q

Action Potentials Phases
Fill in the blanks:
1. Phase 0: _________
2. Phase 1: _________
3. Phase 2: _________
4. Phase 3: _________
5. Phase 4: _________

A
  1. depolarization
  2. brief repolarization
  3. repolarization
  4. resting membrane potential
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15
Q

How is the resting membrane potential (RMP) determined?

A
  • Channels pump ions in a way that creates an ion gradient
    - Sodium-Potassium ATPase
    - 3 Na+ moved out (extra-cellular)
    - 2 K+ moved in (intra-cellular)
  • Overall net negative inside the cell
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16
Q

Resting Membrane Potential
There is typically high concentration of _____(1)________ inside the cell and high concentration of ___(2)___ outside the cell

A
  1. Potassium
  2. Sodium
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17
Q

Action Potential: Cardiomyocyte and Purkinje
Fill in the blanks for the phases of the action potentials:
- Phase 0:____________
- Phase 1:____________
- Phase 2:____________
- Phase 3:____________
- Phase 4:____________

A
  • Na+ channels open (in) => depolarization
  • K+ channels open (out) => brief repolarization
  • Ca2+ channels open (in) => plateau
  • K+ channels open (out) => repolarization
  • returns to RMP
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18
Q

Action Potential: Pacemaker Cells
Fill in the blanks for the phases of the action potentials:
- Phase 4: ____________
- Phase 0: ____________
- Phase 3: ____________

A
  • RMP with automatic “drift” => depolarization
  • Ca2+ channel open (in)
  • K+ channels open (out) => repolarization
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19
Q

Sodium Channels
What determines the cell-to-cell conduction velocity?

A

Slope of Phase 0

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20
Q

Sodium Channels (Phase 0)
Is a type of Na+ channel blocker that helps treat arrhythmias

A

Lidocaine

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21
Q

Definition:
Heart rhythm disturbance

A

arrhythmia

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22
Q

(T/F) Ca2+ is extremely important in all cardiac cells

A

True

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23
Q

Calcium Channels
- T-type (transient) - activated 1st (-60/-50 mV)
- L-type (long-lasting) - activated 2nd

A

Voltage-gated

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24
Q

Calcium Channels
- Norepinephrine and Epinephrine

A

Ligand-gated
- Beta-receptor stimulation increases Ca2+ influx

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25
Q

Drugs:
- Directly block L-type Ca2+ channels
- Diltiazem (heart & vascular) -> treat arrhythmias
- Amlodipine (vascular) -> treat high blood pressure

A

Ca2+ channel blockers

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26
Q

Drugs:
- Indirectly decrease Ca2+ influx and catecholamine effects n the heart
- Atenlol,, esmolol, carvedilol, many others -> treat arrhythmias and other heart diseases

A

Beta-blockers

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27
Q

List the Functions of Potassium Channels:

A
  • Help regulate RMP and repolarization
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28
Q

What channels determine the speed of repolarization & the effective refractory period (ERP)?

A

K+ channels

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29
Q

What would happen to the ERP when you block K+ channels?

A

Increases the ERP & slows repolarization

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30
Q

What represents the sum of all the individual cells’ electrical activity?

A

ECGs

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31
Q

A brief intro to ECG:
What waveform is the following describing?
Atrial depolarization

A

P wave

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32
Q

A brief intro to ECG:
What waveform is the following describing?
Ventricular depolarization

A

QRS wave

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33
Q

A brief intro to ECG:
What waveform is the following describing?
Ventricular repolarization

A

T wave

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34
Q

Serum potassium affects potassium channels:

A

go back

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35
Q

What creates an RMP?

A

Polarization of cardiac cells
- polarization allows cells to become activated (depolarized) and inactivated (repolarized) by movement of different ions across channels

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36
Q

What creates the automatic drift in pacemaker cells?

A

Funny current

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37
Q

(T/F) High extracellular K inactivates Na channels

A

True

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38
Q

What is responsible for the repolarization of Purkinje/cardiomyocytes and pacemaker cells?

A

Potassium

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39
Q

(T/F) Parasympathetic activity increases heart rate and AV nodal conduction

A

False, Sympathetic activity increases heart rate and AV nodal conduction

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40
Q

(T/F) Ultrastructural components and channels of the sarcomere control calcium influx and ultimately myocardial contraction

A

True

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41
Q

What is the main ion responsible for the repolarization of Purkinje/cardiomyocyte cells?

A

Potassium (moving out of the cell)

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42
Q

Enhanced sympathetic tone causes:
A. pacemaker cells to fire more rapidly
B. slows AV nodal conduction
C. pacemaker cells to fire more slowly
D. slower heart rate

A

A. pacemaker cells to fire more rapidly

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43
Q

What is the main ion responsible for the depolarization of Purkinje/cardiomyocyte cells?

A

Sodium (moving into the cell)

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44
Q

(T/F) The resting membrane potentials for Purkinje cells and pacemakers cells are normally negative

A

True

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45
Q

Which is true regarding hyperkalemia and the action potential?
A. Hyperkalemia causes the resting membrane potential to be more negative (hyperpolarized).
B. Hyperkalemia speeds up pacemaker activity.
C. Hyperkalemia causes sodium channels to become inactivated.
D. Hyperkalemia causes repolarization to occur more slowly.

A

C. Hyperkalemia causes sodium channels to become inactivated.

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46
Q

The following sequence of events are related to excitation-contraction coupling in cardiomyocytes. Arrange the following events in the correct sequence from start to end:
1. calcium ions move into the sarcoplasmic reticulum
2. sodium enters into the cell during ventricular activation
3. intracellular calcium stores are released via activation of the ryanodine receptor from the sarcoplasmic reticulum
4. calcium ions move inward across the L-type calcium channel
5. binding of calcium by cTnC allows actin-myosin interaction

A

2 -> 4 -> 3 -> 5 -> 1

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47
Q

** FILLER CARD **

A

C3

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48
Q

Myocardial Contraction
Definition:
Associated with increased muscle tension & pumping of blood into the systemic circulation

A

Period of contraction (= systole)

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49
Q

Myocardial Contraction: Period of contraction (= systole)
List the Essential components:

A
  • Actin
  • Myosin
  • ATP (O2)
  • Calcium => absolutely important
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50
Q

Definition:
Containing tight junctions and gap junctions link adjacent cells

A

Intercalated discs
- Allows rapid spread of electrical signal for simultaneous regional contraction

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51
Q

What is the Functional unit of the myocardium?

A

Sarcomere
- Hypertrophic cardiomyopathy (in cats) => Sarcomere mutation

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52
Q

Myocardial contraction:
Thin actin filaments slide between thick myosin filaments as a result of what?

A

Repetitive movements of the myosin head

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53
Q

Definition:
The linkage between myosin head and actin

A

Crossbridge
- Crossbridge cycle is repetitive attachment | detachment of myosin heads to and from actin filament triggered by arrival of Ca2+

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54
Q

Definition:
Rate (velocity) and Extent (tension or force developed) of fiber shortening

A

Myocardial contractility
- Intrinsic ability (no outside force) of cardiomyocytes to generate force that is load-independent

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55
Q

Definition:
Strength of contraction

A

inotropy

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56
Q

Definition:
Active, energy-requiring process

A

Contraction
- Transformation of chemical energy -> mechanical work
- Splitting ATP by hydrolysis

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57
Q

(T/F) Myocardial contractility can only be assessed using muscle strip preparations (Langendorff technique)

A

True

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58
Q

Myocardial Contractility
- Difficult to measure
- Load-independent (inherent) rate & strength of actin-myosin interaction modulated by Ca2+ availability and sensitivity
- Estimated by velocity of muscle strip (Vmax) at zero load – not measurable in patients
- Inotropy increases with increased availability of Ca2+
- Inotropy increases with increased preload (fiber stretch, before contraction kicks in) – proportional
- Intropy decreases with increased afterload (forces opposing contraction) – inversely proportional
- Inotropy increases with increased heart rate – proportional

A

Inotropic State (contractility)
- it is all about calcium (and ATP)

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59
Q

(T/F) Normally in a resting state, the Ca2+ concentration in the cardia cytosol during systole is such that the contractile sites are approximately half activated

A

True
- Contractile reserve => exploited by sympathetic (beta-adrenergic) stimulation which increases Ca2+ release

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60
Q
  • Positive inotropy (+ positive chronotropy)
A

Sympathetic (NE, Epi)

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61
Q
  • Negative inotropy (+ negative chronotropy)
A

PNS (vagus)

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62
Q

List the Effects of Preload on myocardial Contractility:

A
  • End-diastolic fiber stretch = preload
  • Modulates sarcomere (Z-Z) length before contraction
  • 2 significant effects of increased preload:
    - increased Sensitivity of cardiac tropin C to Ca2+
    - increased Number of cross-bridges
  • Length- tension relationship (Frank-Starling law of the heart)
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63
Q

Clinical Pointe:
What is a variable of preload that influences contractility?

A

Cardiac chamber size (end-diastolic volume)

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64
Q

Definition:
For the same amount of filling (preload), volume pumped per beat is decreased

A

Depressed inotropy

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65
Q

List the Effects of Afterload on Myocardial Contractility:

A
  • All forces opposing muscle shortening (and thus ejection of blood)
  • Weight must be overcome and moved as the muscle shortens
  • The higher Afterload (AL), the higher the tension that must develop prior to actual shortening
  • increased afterload: both muscle shortening and duration of contraction decrease
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66
Q

(T/F) Afterload of the intact ventricle is difficult to measure force that must be overcome in order to open aortic \ pulmonary valves and eject blood into the arterial system

A

True

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67
Q

What does Afterload relate to?

A

Peak wall tension prior to ejection

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68
Q

When does peak wall tension (systolic wall stress) occur?

A

At the ONSET of ventricular ejection

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69
Q

Definition:
Volume of blood in ventricles at end of diastole (end-diastolic pressure)

A

Preload

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70
Q

Definition:
Resistance left ventricle must overcome to circulate blood

A

Afterload

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71
Q

What does increased Heart Rate shorten?

A

Filling time which decreases preload

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72
Q

What is the Shortening fraction?

A

EDD - ESD/EDD x 100%

73
Q

Which of the following statements regarding myocardial contraction and relaxation is CORRECT:
a. During ventricular filling, the semilunar valves are open, and the AV valves are closed
b. During isovolumic relaxation, calcium enters the cardiomyocytes triggering early diastolic cross bridge detachment.
c. During the ejection phase, blood is pumped into the ventricles.
d. During isovolumic contraction, all 4 cardiac valves are closed and ventricular pressure increases.
e. During systole, calcium enters the sarcoplasmic reticulum (SR)and ADP is hydrolyzed. During diastole, calcium leaves the SR into the cytoplasm and is bound to troponin C.

A

d. During isovolumic contraction, all 4 cardiac valves are closed, and ventricular pressure increases.

74
Q

All of the following are characteristics of myocardial contractility, EXCEPT:
a. Rate of cross-bridge cycling
b. Stretch of myofibers
c. Speed (velocity) of contraction
d. Extent of fiber shortening
e. Myofiber tension developed during contraction

A

b. Stretch of myofibers

75
Q

Which of the following statements about myocardial contraction is CORRECT?
a. Ca2+ movement into the SR leads to the power stroke
b. Activation of the PNS increases contractility
c. Ca2+ channel blocking drugs effectively increase Ca2+ sensitivity of troponin C
d. Increased end-diastolic fiber stretch increases contractility
e. Chronic elevation of afterload increases contractile force via the Anrep effect

A

d. Increased end-diastolic fiber stretch increases contractility

76
Q

A dog with chronic mitral valve disease ruptures chordae tendineae of the mitral valve leading to acute, severe mitral regurgitation and subsequent severe left atrial and left ventricular volume overload. All of the following statements regarding changes in LV systolic function are correct, EXCEPT:
a. The event causes massive dilation of the LV leading to increased afterload and thus reducing LV systolic function.
b. The valve leakage causes an acute increase of preload leading to increased systolic function.
c. The SNS will immediately be activated (“fight-or-flight” response) causing increased heart rate and increased cross-bridge cycling.
d. The inotropic state of the myocardium will improve via the Frank Starling mechanism and the Bowditch-Treppe effect.
e. The sarcomere Z-Z length will increase improving the pumping ability of the myocardium.

A

a. The event causes massive dilation of the LV leading to increased afterload and thus reducing LV systolic function.

77
Q

** FILLER CARD **

78
Q

What is the term used to characterize Rate (velocity) & Extent (magnitude) of fiber lengthening

A

Myocardial Relaxation (Lusitropy)

79
Q

Myocardial Relaxation:
Period of cross-bridge ___________ associated with active relief of muscle tension followed by filling of the ventricles

A

Detachment

80
Q

List the Essential components for Myocardial Relaxation:

A
  • SERCA
  • Phospholamban
  • ATP (O2)
  • NCX
  • Ca2+ pump
81
Q

(T/F) Relaxation is very sensitive to hypoxia, ischemia, etc

82
Q

Diastolic Relaxation: Active process (ATP) - O2
It is influenced by …

A
  • Preload
  • Afterload
  • Prior systole
  • Chamber geometry
83
Q

When does cardiomyocyte relaxation occur?

A

Starts after contraction is nearly completed

84
Q

What expels some Ca2+ out of the cell?

A

Na+-Ca2+ exchanger

85
Q

Pumps most of the free Ca2+ back into sarcoendoplasmic reticulum stores where it is bound to calsequestrin

A

SERCA (sarcoendoplasmic reticulum ATPase)

86
Q

Where is some calcium temporarily stored?

A

Mitochondria

87
Q

Definition:
Clinically highly relevant in particular feline heart muscle disease & pericardial disease and other conditions

A

Diastolic Function

88
Q

Diastolic function:
Function that allows adequate filling of the ventricles at rest and during exercise without pathogenic elevation of filling pressure

A

Normal diastolic function

89
Q

Relates relaxation and passive tissue properties to load & chamber geometry

A

Diastolic function

90
Q

(T/F) Diastolic function relates to lusitropy

A

False, Diastolic function doesn’t equal lusitropy (relaxation)

91
Q

Cell lengthening (rate & extent) = _______________ at zero load

A

Relaxation

92
Q

The filling phase follows what phase?

A

Isovolumic (all four cardiac valves are closed) phase

93
Q

List the phases of Diastole:

A
  • IVR (isovolumic ventricular relaxation)
  • Rapid Filling
    - MV open
  • Slow filling
    - MV partially open
  • Atrial contraction
    - = “atrial kick”
    - MV open
94
Q

Ventricular Filling Dynamics:
The early diastolic filling provides _______% of LV filling volume

95
Q

List the effect of preload & Heart rate on diastolic functions:

A
  • increase Preload improves diastolic function (within limits)
  • increase Heart rate improves relaxation & ventricular suction Caveat: decrease filling time & decrease coronary perfusion
96
Q

(T/F) If tau goes down, it means there is a better relaxation

97
Q

Which statement about myocardial relaxation is CORRECT?
a. It is a passive process related to the early diastolic LA-LV pressure difference.
b. It does improve with increased Ca2+ binding to the tropomyosin complex.
c. It is facilitated by the binding of phospholamban to SERCA.
d. It gets faster and stronger with parasympathetic activation.
e. It is a process mainly confined to the isovolumic period in early diastole.

A

e. It is a process mainly confined to the isovolumic period in early diastole.

98
Q

Which of the following sequence of events during cardiac excitation-contraction-relaxation is CORRECT?
1…Ca2+ binding to cardiac troponin C
2… Ca2+ entry via the L-type Ca2+ channel
3… Power stroke
4… Ca2+ extrusion out of the cytoplasm via the Ca2+ pump
5… Temporary Ca2+ storage in the mitochondria
6… Electrical cardiomyocyte activation
7… Ca2+ triggered Ca2+ release
8… Ca2+ flux into the sarcoendoplasmatic reticulum via SERCA

A

b. 6-> 2-> 7-> 1-> 3-> 8-> 4-> 5

99
Q

All of the statements about ventricular diastolic
function are correct, EXCEPT?
a. Diastolic function is an overarching term to describe ventricular filling.
b. Diastolic function can conceptionally be divided into 4 phases occurring in the following sequence: Isovolumic contraction, early filling, late filling, and finally diastasis.
c. Rapid ventricular filling occurs in early diastole and is caused by myocardial relaxation associated with the suction of blood into the ventricle reducing LV pressure and thus the early diastolic LV-LA pressure gradient.
d. Normal diastolic function allows adequate filling of the ventricles without a pathologic elevation of filling pressure.
e. Stiffness (or its reciprocal, compliance) describes the passive diastolic properties of the myocardium (ventricle). The stiffer, the worse is diastolic filling.

100
Q

A cat with severe, idiopathic thickening of the LV walls and a heart rate of 260 bpm (N: 120-220) is diagnosed with hypertrophic cardiomyopathy in your practice via cardiac ultrasound (we will talk about this common feline condition later in the course). Which of the following statements regarding LV diastolic function in this cat is NOT correct?

a. LV compliance will be decreased and thus LV filling reduced.
b. Relaxation of the LV will be abnormal due to increased myocardial mass.
c. High heart rate will make LV filling worse.
d. LV stiffness will be increased affecting LV diastolic (filling) properties.
e. LV stroke volume will be increased due to increased heart rate and better relaxation and thus, better filling, of this thickened heart.

A

e. LV stroke volume will be increased due to increased heart rate and better relaxation and thus, better filling, of this thickened heart.

101
Q

** FILLER CARD **

102
Q

The Cardiac Cycle
- Electrical activity __________ mechanical activity (electromechanical delay)

A

precedes(before)

103
Q

The Cardiac Cycle
How is blood flow predicted?

A

Pressure differences
- “Pressure gradients”
- Flows from higher pressure to lower pressure

104
Q

The Cardiac Cycle
Heart valves open and close in response to _____________ on either side of the valves

A

Pressure changes

105
Q

Wiggers Diagram: Electrical Activity
1. Starts with ECG & ECG is what?

A

Basis of timing (basically your x-axis)

106
Q

Genesis of the ECG
1. Impulse starts in the ___ node

107
Q

Genesis of the ECG
2. Signal traves through atria and ____ node

108
Q

Genesis of the ECG
3. Signal travels through ________________ system

A

His-Purkinje system

109
Q

Genesis of the ECG
4. __________ depolarization

A

Ventricular

110
Q

Genesis of the ECG
5. Ventricular _____________

A

repolarization

111
Q

Wiggers Diagram: Mechanical
- LV ejection
- Isovolumic contraction (IVC)
- Isovolumic relaxation (IVR)

A

Ventricular Pressure/timing

112
Q

Wiggers Diagram: Mechanical
_______ atrial pressure/timing

113
Q

Wiggers Diagram: Mechanical
- MC = mitral closure
- AO = aortic opens
- AC = aortic closure
- MO = mitral opens

A

Valve Motion
- Driven by pressure differences

114
Q

Wiggers Diagram:
Think about ventricular volume as it relates to ___________ & ___________

A

timing, pressure
- Filling
- Ejection
- Isovolumic periods

115
Q

Wiggers Diagram:
Changes in volume between what two points represent stroke volume?

116
Q

Wiggers Diagram: Clinical Aspect (Heart Sounds)
- Closure of atrioventricular valves

A

S1
- Systolic heart sounds

117
Q

Wiggers Diagram: Clinical Aspect (Heart Sounds)
- Closure of semilunar valves (aortic & pulmonary valve)

A

S2
- Systolic heart sounds

118
Q

Wiggers Diagram: Clinical Aspect (Heart Sounds)
- Early/rapid ventricular filling

A

S3
- Diastolic heart sounds

119
Q

Wiggers Diagram: Clinical Aspect (Heart Sounds)
- Atrial contraction (“atrial kick”)
- final phase

A

S4
- Diastolic heart sounds

120
Q

Average Pressures for Species examined (in mmHg)
Systole: 120
Diastole: < 12

A

Left ventricle

121
Q

Average Pressures for Species examined (in mmHg)
Systole: 25
Diastole: < 5

A

Right ventricle

122
Q

Average Pressures for Species examined (in mmHg)
Systole: 120
Diastole: 80

123
Q

Average Pressures for Species examined (in mmHg)
Systole: 25
Diastole: 12

A

Pulmonary artery

124
Q

Clinical correlations:
How is pulse pressure determined?

A
  • Difference in systolic and diastolic pressure
  • Rate of rise of systolic pressure
125
Q

Definition:
Is a persistent opening between the two major blood vessels leading from the heart.

A

Patent ductus arteriosus (PDA)
- Bounding Pulses = aortic insufficiency, patent ductus arteriosus
- difference in systolic and diastolic pressure

126
Q

Definition:
Is a narrowing of the area underneath, the aortic valve, that causes some degree of obstruction or blockage of the blood flow through the heart

A

Subaortic stenosis (narrowing)
- rate of rise of systolic pressure
- Weak pulses

127
Q

Clinical correlations:
What happens when there’s any kind of backup of blood in the superior vena cava or in your heart itself?

A

Distended jugular veins

128
Q

Clinical correlations:
“Cannon waves” with arrhythmias (3rd degree AV block) due to dyssynchrony (atria contracting against closed mitral/tricuspid)

A

Jugular pulsations

129
Q

Clinical correlations:
Slurring between normal heart sounds
- Valve leakage = regurgitation or insufficiency
- Valve narrowing = stenosis

A

Heart Sounds: Murmurs

130
Q

Clinical correlations:
- Diastolic sounds (S3 and S4 sound)
- Normal in large animals
- Abnormal in small animals

A

Heart Sounds: Gallops

131
Q

What occurs immediately prior to the ejection of blood out into the aorta?

A

c. isovolumic contraction

132
Q

List the chambers, and great vessels, and list the normal pressure ranges (in mmHg):

A
  • RA (0-5)
  • RV (25 / <5)
  • PA (25 / 12)
  • LA (0-12)
  • LV (120 / <12)
  • Ao (120 / 80)
133
Q

** FILLER CARDS **

134
Q

Hemodynamics
Definition:
The study of blood flow in the vascular system

A

Hemorheology

135
Q

What is the purpose of the cardiovascular system?

A

To deliver oxygen and nutrients to the tissues of the body

136
Q

Hemodynamics
Cardiac output

137
Q

Hemodynamics
- Ventricular
- Atrial
- Arterial
- Venous
- Capillary

138
Q

Hemodynamics
- Systemic vasculature
- Pulmonary vasculate

A

Resistances

139
Q

Ohm’s Law

A

I = V/R
Q = P/R

140
Q

Ohm’s Law
What is current flow (I) determined by?

A
  • Electromotive force or voltage (V)
  • Resistance to current flow (R)
141
Q

Ohm’s Law
What is the flow of fluids (Q) determined by?

A
  • Pressure gradient (P)
  • resistance to flow (R)
142
Q

Hemodynamics: Physical Laws & Determinants
Physical Law: Venous return
Determinants:

A
  • Plasma volume
  • Vessel capacity
143
Q

Hemodynamics: Physical Laws & Determinants
Physical Law: Cardiac output (CO) –> CO = SV x HR
Determinants:

A
  • Stroke volume (SV) => EDV - ESV
  • Heart rate (HR)
  • Tissue demands
144
Q

Hemodynamics: Physical Laws & Determinants
Physical Law: Blood pressure (BP) –> BP = CO x SVR
Determinants:

A
  • Cardiac output (CO)
  • Systemic vascular resistance (SVR)
  • Reflexes
145
Q

Hemodynamics: Physical Laws & Determinants
Physical Law: Vascular resistance
- Systemic vascular resistance (SVR)
- Pulmonary vascular resistance (PVR)
Determinants:

A
  • Autonomic nervous system
  • Hormonal & endothelial (local) regulations
    –> PVR = about 1/5 of SVR
146
Q

Definition:
The flow of blood from the periphery back to the right atrium

A

Venous return

147
Q

Venous Return:
“Force from the rear”

A

Cardiac pumping from the contralateral ventricle
- LV pumping blood into the arterial system

148
Q

Venous return:
“Force from the front”

A

Force from ventricular contraction creates negative pressure in the atrium

149
Q

Venous Return: Respiratory Pump
Inspiration causes the diaphragm to move downward causing negative pressure in the chest and _________ atrium

150
Q

Venous Return:
Influence of Fluid Therapy
How can you improve venous return?

A

with fluid bolus

151
Q

Venous Return:
Influence of Fluid Therapy
What drives blood into the right atrium?

A

Mean systemic venous pressure
- Mean systemic venous pressure > RA pressure = venous return

152
Q

List the things that increase (improve) venous return:

A
  • Vasoconstriction
  • Splenic contraction
  • Fluids
153
Q

Definition:
- Quantity of blood delivered to the systemic circulation per unit time (L/min)
- Converted to cardiac index (CI)
- Normalize to patient size (body surface area)
- L/min/m^2

A

Cardiac Output

154
Q

Cardiac Output:
End diastolic (filling) volume - End systolic volume

A

Stroke volume

155
Q

Cardiac Output:
List the thing that will affect End diastole volume:

A
  • Preload
  • Compliance
  • Diastolic filling time
156
Q

Definition:
how easily a chamber of the heart or the lumen of a blood vessel expands when it is filled with a volume of blood

A

Compliance

157
Q

Cardiac Output:
List the thing that will affect End systolic volume:

A
  • Contractility (pump function)
  • Afterload
158
Q

Cardiac Output:
Distending stress in the ventricle at end-diastole; depends on venous return & ventricular compliance

159
Q

Cardiac Output:
What is dependent on HR (autonomic tone)?

A

Diastolic Filling Time

160
Q

Cardiac Output:
The sum of the forces opposing the ventricular ejection (blood pressure, vascular resistance)

161
Q

List the determinants for Arterial Blood Pressure (BP = CO x SVR):

A
  • Blood volume (CO, SV)
  • Compliance of vessels (vascular resistance)
  • Baroreceptor arcs (reflexes)
    - Stabilize BP in face of changing CO
162
Q

(T/F) Mean arterial pressure (MAP) more important than systolic/diastolic

A

True
MAP = 1/3 pulse pressure + diastolic blood pressure (pulse pressure = systolic - diastolic)
** this is important and you should know **

163
Q

What are the two ways to measure pressure non-invasive (indirect)?

A

Doppler & Oscillometric

164
Q

Arterial Blood Pressure:
- Gold-standard
- Recommended for severely hypo/hypertensive patients to guide therapy

A

Invasive (direct) way to measure Arterial Blood Pressure

165
Q

Arterial Blood pressure:
- Are important ways that the body can regulate blood pressure
- Important & normal reflex that occurs

A

Baroreceptor Reflex

166
Q

An exaggeration of the normal baroreceptor reflex can result in what?

A

Syncope (collapse)
- Vasovagal syncope
- Neurcardiogenic syncope
- Reflex-mediated syncope
* all the same thing
–> this exaggeration can cause severe bradycardia & hypotension

167
Q

Vascular resistance equation:

A

Flow (or CO) = change in Pressure / Resistance

168
Q

(T/F) Flow (CO) can be reduced, although BP increases

A

True
- RESISTANCES can Change

169
Q

Vascular Resistance:
Opposition to flow presented by pulsatile flow in an elastic vascular system

A

Impedance
- Wave reflection
- difficult to quantify

170
Q

Vascular Resistance:
What percentage does Resistance make up of impedance?

171
Q

Vascular Resistance:
Resistance of the systemic vascular tree (arterioles)

A

Systemic vascular resistance

172
Q

Vascular Resistance:
Resistance of the pulmonary vascular tree

A

Pulmonary vascular resistance (PVR)

173
Q

Poiseuille’s Law

A

Resistance = 8 x length x viscosity / pi x radius^4
- Resistance increases EXPONENTIALLY when vessel radius narrows

174
Q

List the factors affecting resistance:

A
  • Autonomic nervous system
  • Hormonal and endothelial (local) factor
175
Q

If a vessel diameter decreases by half, by what factor would the vascular resistance increase?

176
Q

(T/F) Flow is inversely proportional to resistance

177
Q

(T/F) Flow is inversely proportional to the pressure difference (pressure gradient)

178
Q

Which statement is true regarding venous return and respiration?

a. Inspiration increases overall intrathoracic pressure in the chest causing blood to move out of the right atrium into the vena cava.
b. Expiration increases intrathoracic negative pressure causing an increase in venous return.
c. Inspiration increases intrathoracic negative pressure lowering the pressure in the right atrium.
d. An increase in right atrial pressure as compared to the vena cava causes an increase in venous return.

A

c. Inspiration increases intrathoracic negative pressure lowering the pressure in the right atrium.

Cardiology (SP23) (8 decks)

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