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Cardiovascular System > Physiology2 > Flashcards

Physiology2 Flashcards

1
Q

Frank-Starling Graph

A
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2
Q
A
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3
Q

Diastolic response: length/volume vs pressure

A

There is little increase in pressure as the end-diastolic volume increases until the end (isometric contraction), at the end the fibers are all stretched out. Passive pressure since ventricle not contracting.

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4
Q

Systolic response: length/volume vs. pressure

A

Fast increase in pressure as volume decreases then levels off as fibers contract because the fibers are overextended at higher pressure. Then there is ejection and a decrease in pressure as the blood exits and the pressure is equalized to atrial pressure. The pressure is a measure of contractile force.

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5
Q

What is preload?

A

Increased length of fibers/ventricular wall stress/increased filling pressure of ventricles at end diastolic volume.

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6
Q

What is afterload?

A

Aortic pressure during ejection period/aortic valve opening. Resistance to what is being pushed out by the ventricle so afterload is inversely proportinoal to pressure in ventricles. Refers to the load that the perloaded muscle has to work against.

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7
Q

Laplace’s law and wall stress

A

WS=Pxr/(2*wall thickness) or σ = P.r/ 2h. Explains thickening of arteries and ventricles. Wall stress during systolic ejection is equivalent to the afterload. Pressure in equation can be estimated from arterial systolic pressure.

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8
Q

How does aortic diastolic pressure relate to the afterload?

A

Aortic pressure already exists (due to HTN, etc) even though valve hasn’t opened yet. Heart needs to pump harder to push blood against this resistance. A higher aortic pressure means more afterload.

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9
Q

What happens to pressure as afterload (aortic pressure) increases with preload constant?

A

Increases with constant slope until the pressure of the aorta is equal to that in the ventricle and there is no bloodflow–>heart failure. Essentially the effect of essential hypertension.

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10
Q

What happens to the pressure vs afterload graph with an increased preload?

A

Same graph but moved up, the left ventricular pressure developed at all points will increase and the new curve will be parallel and on top of the original one. Peak isometric force will be reached at a higher level and a change in peak isometric force versus initial fiber length (preload) will have occurred. NOT a change in contractility.

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11
Q

Contractility definition

A

Change in peak isometric force vs. initial fiber length (EDV). Intrinsic property of the cardiac cell that defines the amount of work that the heart can perform at a given load. Determined by availability of intracellular Ca2+.

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12
Q

Contractility in a normal heart vs Norepinephrine and Heart Failure (Graph)

A
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13
Q

What is the effect of heart failure on pumping?

A

Decreases contractility, works with a higher preload due to a reduced ventricular ejection and high blood volume due to fluid retention.

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14
Q

How does diminished heart failure cause CHF?

A

HTN causes Back pressure in LA, into pulmonary vein, into lungs, fluid in lungs (alveoli), CHF

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15
Q

How does the change in left ventricular pressure over time change with failing heart or with epinephrine?

A

Epinephrine increases contractility and also ventricular pressure/instantaneous change in time. Failing heart has lower contractility and lower change in ventricular pressure/time.

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16
Q

What is S1?

A

AV valves closing during early ventricular contraction

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17
Q

S2?

A

Semilunar valves closing during early ventricular relaxation

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18
Q

Heart sounds graph with time and ventricular phases

A
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19
Q

Mechanism of aortic stenosis

A

Pressure doesn’t rise high enough to open aortic valve all the way and valve is difficult to open because it’s hard. Ventricle contraction presses on aortic valve and aortic pressure will not rise with ventricular pressure.

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20
Q

What is the area under the pressure/volume loop?

A

Measure the work performed by the ventricle

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21
Q

Cardiac cycle beginning with mitral valve opening:

A

Mitral valve opening-filling-mitral valve closing-isovolumic contraction-aortic valve opening-rapid ejection phase-slow ejection phase-aortic valve closing-isovolumic relaxation-mitral valve opening

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22
Q

What happens if the afterload and contractility are constant but preload is increased (as in IV)?

A

Left ventricle EDV will rise, stroke volume will increase by Frank-Starling mechanism and ESV will be the same.

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23
Q

What is the effect of a hypertrophied ventricle on the pressure/volume curve?

A

Increases slope of diastolic filling curve, EDV is decreased. If afterload and contractility remain constant, SV is reduced.

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24
Q

What happens if the preload and contractility are kept constant but afterload is increased ( as in hypertension or aortic stenosis)?

A

Pressure generated by LV increases, more ventricular work is used to overcome resistance to ejection. Less fiber shortening takes place. Increased LV-ESV. Stroke volume is reduced.

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25
Q

What is the relationship between ESV and afterload in the End Systolic Pressure Volume Relation (ESPVR)?

A

Linear increase. A measure of cardiac contractility.

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26
Q

What happens to the ESPVR slope when contractility is reduced like high dose Beta blocker therapy or dilated cardiomyopathy associated to cardiac failure?

A

Reduced

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27
Q

What is ESV dependent on?

A

Contractility and afterload. NOT EDV.

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28
Q

Stroke work output of the heart definition

A

Amount of energy that the heart converts to work during each heartbeat while pumping blood into the arteries.

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29
Q

Minute work output definition

A

Total amount of energy converted to work in 1 minute, stroke work output × heart rate.

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30
Q

Volume-pressure work or External work definition

A

Used to move the blood from the low-pressure veins to the high-pressure arteries. Includes only blood ejected from heart.

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31
Q

Kinetic energy of blood flow or internal work definition

A

Used to accelerate the blood to its velocity of ejection through the aortic and pulmonary valves. Includes blood remaining in the heart.

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32
Q

How does a poorly drained LV during cardiopulmonary bypass affect the internal and external work?

A

External work provided by roller pump but since there is still blood in the LV, tension builds and can create myocardial ischemia.

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33
Q

Efficiency of Cardiac Contraction definition

A

The ratio of work output to total chemical energy expenditure. Maximum efficiency of the normal heart is between 20 and 25%, in HF 5-10%.

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34
Q

What are the 4 phases of diastole?

A

Isovolumic relaxation, Rapid filling phase, Slow filling or diastasis, Atrial systole.

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35
Q

Extrinsic Factors determining distensibility

A

Pericardium, Right Ventricle, Intrapleural & Mediastinal Pressures, Coronary vascular volume

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36
Q

Physical properties of LV determining distensibility

A

Ventricular geometry (Volume, Wall thickness), Composition of ventricle wall

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37
Q

Myocardial Relaxation determination of LV distensibility

A

Load, Inactivation of actin myosin crosslinks, Spatial & Temporal nonuniformity

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38
Q

What are the causes of passive cardiac chamber stiffness?

A

Fibrosis, cellular disarray, hypertrophy

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39
Q

What are the possible causes of decreased cardiac relaxation?

A

Hypertrophy, Asynchrony, abnormal loading, ischemia, abnormal calcium ion flux.

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40
Q

What are the two components leading to increased diastolic pressure?

A

Increased passive chamber stiffness and decreased relaxation

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41
Q

Table of conditions involving diastolic HF

A
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42
Q

Methods of measuring diastole function

A

Transmitral pulsed wave doppler flow pattern, Pulmonary vein 2-D doppler flow pattern, Color M-mode doppler Echocardiography, Tissue doppler Echocardipgraphy

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43
Q

Effect of Paced HR on Diastolic Pressure and Volume in normal vs Coronary artery disease

A

Increased HR means lower EDV (worse in coronary artery disease), increased ESPVR and lower pressures in normal coronaries. In CAD it causes decreased pressures (but CAD caused overall higher pressures). In normal coronaries, higher heartrate decreases ESV but the ESV is equally low in all HRs in CAD.

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44
Q
A
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45
Q

What is the effect of revascularization on diastolic dysfunction? (Graph of Pressure/Volume after ischemia)

A
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46
Q
A
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47
Q

Phases of systole

A

Isovolumic Contraction, Period of rapid ejection, Period of slow ejection

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48
Q

Definition of systole

A

Ejection of blood into circulation via generation of a pressure gradient

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49
Q

Cardiac output (CO) definition

A

Amount of blood flowing into circulation per minute

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50
Q

Calculation of CO

A

CO=HRxSV

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51
Q

Normal value of CO

A

5-6L/min

52
Q

Secondary factors of CO

A

Venous return, Systemic vascular resistance, Peripheral oxygen use, Total blood volume, Respiration, Body position

53
Q

Cardiac index formula

A

CI=CO/BSA (body surface area)

54
Q

Normal value of Cardiac index

A

2.5-3.5 L/min/m^2

55
Q

Fick Principle formula for Cardiac Output

A

O2 consumption (mL/min)/(PvO2-PaO2)

56
Q

Fick Principle Definition

A

Based on law of conservation of mass. Oxygen in pulmonary veins must equal the sum of oxygen coming in from the alveoli plus that in the pulmonary arteries.

57
Q

Stroke volume (SV) definition

A

Amount of blood ejected by ventricle with each single contraction.

58
Q

Formula for SV

A

SV=EDV-ESV

59
Q

Determinants of stroke volume

A

Preload, Afterload, Contractility.

60
Q

What can be substituted approximately for preload?

A

Ventricular volumes for preload stress (EDP, LAP, PCWP, PDP, RAP, CVP), ventricular pressure for ventricular volumes (EDV).

61
Q

Factors affecting preload

A

Total blood volume, Body position, Intrathoracic pressure, Intrapericardial pressure, Venous tone, Pumping action of skeletal muscle, Atrial contribution of ventricular filling.

62
Q

Methods to measure LVEDV

A

TEE, Ventriculography, radionuclide scans, conductance catheters.

63
Q

Methods to measure LVEDP

A

LAP, PCWP, PADP, CVP

64
Q

What is the relationship between the Frank-Starling Curve and SV

A

With increasing diastolic muscle fibre length, SV increases steadily. Once limit of preload reserve (sarcomeres are at their optimal length), SV cannot be further enhanced.

65
Q

Graph of family of Starling Curves (Normal, exercise, HF)

A
66
Q

Definition of afterload

A

Stress imposed on ventricular wall during systole. Arterial impedance to ejection of SV.

67
Q

Measurements of afterload

A

Wall stress, Impedence, Effective arterial elastance, Systolic intraventricular pressure, Systemic vascular resistance, Pulmonary vascular resistance

68
Q

Wall stress definition

A

Burden that the LV or RV has to shoulder for ejecting the SV. Quantified by the Laplace equation. Stress at end systole is used because it heralds end of LV force development beyond which muscle fibre stop shortening.

69
Q

When is peak wall stress?

A

Within the first one-third of ventricular ejection. Declines throughout the remainder of systole.

70
Q

How does the end systolic wall stress compared to the peak wall stress?

A

σes < 50% of its peak value.

71
Q

When is the peak systolic wall stress the most important stimuli for LVH?

A

Chronic pressure overload states such as systemic hypertension, valvular aortic stenosis, or coarctation of the aorta

72
Q

How is wall stress used as a determinant of myocardial oxygen requirements?

A

Integral of left ventricular systolic wall stress over time (along with HR and contractile state).

73
Q

End systolic wall stress definition

A

σes which defines the limiting force to left ventricular fiber shortening. Ventricular ejection ends when instantaneous myocardial force reaches the maximal or isometric value for the existing chamber size, thickness, and pressure.

74
Q

How does the overall extent and mean velocity of fiber shortening relate to σes?

A

For a given contractility they are inversely related.

75
Q

Systemic vascular resitance definition

A

Ratio of pressure to flow at zero frequency (non pulsatile flow). Used for treatment of afterload reduction for LV or RV failure.

76
Q

How are CO and SVR related?

A

Inverse ration

77
Q

Equation for systemic vascular resistance

A

SVR = [MAP – RAP] /CO

78
Q

Effective Arterial Elastance Definition

A

Pressure to volume ratio at end systole. Mechanical characteristic of vascular system.

79
Q

Systolic Intraventricular Pressure definition

A

Important component of afterload Inverse ratio of SV & LV pressure.

80
Q

Factors increasing contractility

A

Sympathetic stimulation: Direct increases of the force of contraction, Indirect increases due to increased heart rate (rate treppe effect or Bowditch phenomenon). Parasympathetic inhibition. Administration of positive inotropic drugs.

81
Q

Factors decreasing contractility

A

Parasympathetic stimulation (Decreased rate effect), Sympathetic inhibition (Withdrawal of catecholamines Blockade of adrenergic receptors), Drugs (β-adrenergic–blocking drugs Calcium channel blockers Other myocardial depressants), Myocardial ischemia and infarction, Intrinsic myocardial diseases (Cardiomyopathies), Hypoxia and acidosis.

82
Q

Load dependent indices of contractility

A

Isovolumic Contraction Phase Indices: Mean rate of LV pressure rise (Peak dP/dt), Isovolumic contraction time. Ejection Phase Indices: CO, SV, EF, Fractional fibre shortening, Fractional area change.

83
Q

Load-Independent Indices of contractility

A

End systolic pressure volume relationship, Preload recruitable stroke work, Isovolumic myocardial acceleration.

84
Q

What is the most variable determinant of ESPVR?

A

Heart rate

85
Q

Which systems control the heart rate?

A

cardiac conduction system, central nervous system, autonomic nervous system, pharmacologic controls.

86
Q

What are the effects of increasing HR on cardiac function?

A

Shortening of systole, Shortening of diastole: (Decreased myocardial perfusion time, Decreased ventricular filling, Rate dependent change in SV), Rate dependent change in cardiac output, Rate dependent positive inotropic effect.

87
Q

Right ventricular function definition

A

More complex with phases of contraction, Better suited to eject large volumes of blood, More sensitive to afterload, Less sensitive to preload.

88
Q

How is the right ventricle function different from the left?

A

More complex with phases of contraction, more susceptible to lower stroke volume with (more sensitive to) increased afterload and less sensitive (less responsive to increase stroke work) to preload.

89
Q

Where does sympathetic innervation to the heart come from?

A

Upper thoracic ganglia (T2-T5) via superficial & deep cardiac plexus.

90
Q

Where does sympathetic innervation predominate in the heart?

A

In the ventricle (more than atrium)

91
Q

What is the neurotransmitter for sympathetic innervation in the heart?

A

Norepinephrine

92
Q

What are the adrenoreceptors on the heart?

A

α1, α2, β1 and β2

93
Q

What are the actions of sympathetic innervation of the heart?

A

↑ Chronotropy, ↑ Inotropy (α1A, α1B, β1 and β2), Presynaptic inhibition of NE release (α2A)

94
Q

Graph of the effect of sympathetic stimulation on CO and RAP

A
95
Q

What is the main source of parasympathetic innervation to the heart?

A

Vagus nerve

96
Q

Which tissue receives more vagal parasympathetic innervation?

A

Supraventricular tissue (more than ventricles)-SA and AV node particularly

97
Q

What is the neurotransmitter of parasympathetic innervation?

A

Acetylcholine

98
Q

Which receptors receive parasympathetic innervation?

A

Muscarinic: M2- predominant subtype, M3- coronaries

99
Q

Actions of parasympathetic innervation?

A

Reduces pacemaker activity, Slows AV conduction, Decreases the atrial contractile force directly, Exerts inhibitory modulation of ventricular contractile force.

100
Q

Hormones affecting cardiac function-table

A
101
Q
A
102
Q

Location of baroreceptors

A

Wall of carotid sinus and aortic arch

103
Q

What is the role of the baroreceptor reflex?

A

Responsible for the maintenance of blood pressure, Important role during acute blood loss and shock.

104
Q

What is the role of volatile anesthetics (halothane) on the baroreceptor reflex?

A

Inhibits the heart rate component

105
Q

What is the role of calcium channel blockers and ACE inhibitors on the baroreceptor reflex?

A

Lessens cardiovascular response (increase contractility, drop HR, relax smooth muscle)

106
Q

What is the baroreceptor response in patients with chronic hypertension (especially in surgery)?

A

Decreased response leading to perioperative circulatory instability.

107
Q

What mediates the chemoreceptor reflex?

A

Chemosensitive cells in the carotid bodies and the aortic body. Sinus nerve of Hering and vagus nerve, Chemosensitive area of the medulla.

108
Q

in what conditions do the chemoreceptors react?

A

At PaO2

109
Q

What is the chemoreceptor reflex response?

A

Respiratory centers stimulated and increasing ventilatory drive. Activation of the parasympathetic system: reduction in heart rate and myocardial contractility.

110
Q

What elicits the Bainbridge reflex?

A

Stretch receptors located in the right atrial wall and the cavoatrial junction, vagal afferent signals, Cardiovascular center in the medulla.

111
Q

What is the Bainbridge reflex?

A

Increase stretching in the right atrium causes increase in HR to redistribute blood.

112
Q

What elicits the Bezold-Jarisch Reflex?

A

chemoreceptors and mechanoreceptors within the LV wall, Vagal afferents, ↑ parasympathetic tone.

113
Q

What does noxious ventricular stimuli induce in the Bezold-Jarisch Reflex?

A

Triad of hypotension, bradycardia, and coronary artery dilatation.

114
Q

What are cardiovascular implications the Bezold-Jarisch Reflex?

A

Myocardial ischemia or infarction, Thrombolysis, Revascularization, Syncope.

115
Q

What cardiac conditions diminish the Bezold-Jarisch Reflex?

A

Cardiac hypertrophy, Atrial fibrillation.

116
Q

What does the Valsalva maneuver do?

A

↓CO and BP in the baroreceptors, cutting off venous return to thorax.

117
Q

What is the response during the Valsalva maneuver?

A

Sympathetic stimulation, ↑heart rate and myocardial contractility.

118
Q

How is the Valsalva maneuver released?

A

Opening of the glottis.

119
Q

What is the result of the increased venous return after the release of the Valsalva maneuver?

A

Increased blood pressure sensed by the baroreceptors, stimulate parasympathetic efferent pathways to the heart.

120
Q

What is the cause of the Cushing Reflex?

A

Cerebral ischemia or TBI at the medullary vasomotor center

121
Q

What is activated in the Cushing Reflex?

A

Increased sympathetic response: ↑ HR, BP, and myocardial contractility initially to overcome resistance in the head.

122
Q

What is the result of the Cushing reflex?

A

High arterial pressure activates the baroreceptors–>bradycardia.

123
Q

When does the Oculocardiac reflex occur?

A

During 30-90% of ophthalmic surgeries.

124
Q

What mediates the oculocardiac reflex?

A

Nerve connections between the Ophthalmic division of the trigeminal cranial nerve (from stretch receptors near the eyeball through the short and long ciliary nerves) and the vagus nerve of the parasympathetic nervous system through the Gasserian ganglion.

125
Q

What is the result of the Oculocardiac reflex?

A

Increased parasympathetic tone, bradycardia.

Cardiovascular System (28 decks)

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