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Final Review > Hemodynamics > Flashcards

Hemodynamics Flashcards

1
Q

Hemodynamics Definition

A

Study of forces and pressures that influence circulation of the blood

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2
Q

Main Routes to collect Hemodynamic Information

A

Arterial Lines-For the information about the systemic system and perfusion

Central Lines-For information about fluids balance and function of the right heart

Pulmonary Artery Lines-For information about the pulmonary system, fluid balance and the function of the left heart

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3
Q

Liquids

A

Liquids are incompressible

A contained liquid (ex. blood in the body) will have a pressure that is the same for all point at the same level within that liquid

Pressure will vary in a vertical position

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4
Q

Pascal Principals

A

Pascal Principals: A change in the pressure applied to an enclosed fluid is transmitted undiminished to every portion of the fluid and to the walls of the containing vessel

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5
Q

Applying Pascal’s Principle-Blood Pressure

A

If measure BP anywhere in the arterial system it should all be the same as it’s one continuous column of blood. Therefore BP measured at the radial, brachial, femoral or dorsalis pedis should all give the same pressure. (until something changes, such as positioning.)

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6
Q

The Heart As Two Pumps

A

Think of the heart as two pumps where the right receives blood from the venous system and pumps out to the lungs and the left receives blood from the pulmonary system and pumps the blood to the body.

Normally the right and left will receive and pump the same amount of blood

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7
Q

Applying Pascal’s Principle-Arterial Lines

A

When monitoring arterial blood pressure with a transducer connected to an arterial catheter via fluid filled pressure tubing, any changes in the arterial blood pressure are transmitted throughout the fluid filled line and are recorded by the transducer

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8
Q

Ohms Law-Electrical

A

Voltage = Current X Resistance

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9
Q

Ohms Law-Fluids

A

Pressure = Flow X Resistance

P= Driving Pressure

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10
Q

Resistance in the Left Heart Equation (Delta P)

A

Resistance = Delta P / Flow

P= BP =SVR X CO

P= Driving Pressure of the left side of the heart

CO=flow

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11
Q

Systemic Vascular Resistance-Equation

A

SVR= [(MAP-CVP) / CO] X 80

According to this formula the driving pressure is MAP minus CVP. The 80 is a conversion factor that is used so that your answer will be in dynes*sec/cm^-5

Systemic means start in aorta (MAP) and goes to the right atrium (CVP)

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12
Q

FACTORS THAT INCREASE SVR

A
  • Lt heart failure:
    • CHF, cardio, hypovolemic & obstructive shocks
  • Vasoconstricting Agents
    • Examples: Dopamine, Epinephrine, Norepinephrine (Levophed)
  • Hypovolemia
  • Septic shock (late stages)
  • Decreased PaCO2
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13
Q

FACTORS THAT DECREASE SVR

A
  • Neurogenic shock
  • Vasodilating agents
    • Ex. Nitroglycerin, Morphine
  • Septic Shock (early stages)
  • Spinal shock
  • ­ PaCO2
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14
Q

PVR-Equation

A

PVR= ((MPAP-PAWP)/CO) x 80

According to this formula the driving pressure is MPAP minus PAWP.

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15
Q

FACTORS THAT INCREASE PVR

A
  • Right-Sided Heart Failure:
    • Pulmonary hypertension
    • Pulmonary embolism
  • Decreased
    • Alveolar oxygenation
      • Hypoxemia will cause pulmonary vasoconstriction
    • pH
      • Acidosis
    • PaCO2
  • Hyperinflation of Lungs
  • Vascular bloackage, vascular compression
  • Tumor/Mass
  • Vascular destruction
  • Emphysema
  • PIF
  • Pneumo/hemothorax
  • Vasocontrictors
  • PPV/PEEP
    • We are pushing air into the lungs making the air sac get bigger from the inside which will compress blood vessels
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16
Q

FACTORS THAT DECREASE PVR

A
  • Increase in
    • Alveolar oxygenation
    • pH
      • Alkalosis
  • Decrease
    • PaCO2
  • Pharmacological Agents
    • Ca++ channel blockers (‘ol)
  • Humoral Substances
    • Eg. Prostaglandin E
  • Inhaled Nitric oxide
    • This is a vasodilator
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17
Q

Cardiac Output Definition

A

The amount of blood that is pumped out of each ventricle. The cardiac output of the right and left ventricle is equal and identical over a period of time

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18
Q

Cardiac Output Equation

A

CO= (HR x SV)

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19
Q

What is cardiac output determined by

A
  • Cardiac output is determined through a complex set of interrelated physiological variables
    • Preload: The volume of blood in the heart
    • Afterload: The downstream resistance to ejecting blood from the heart
    • Contractility and compliance of the heart muscle
    • Metabolic requirements of the body
  • A single CO measurement will represent the interaction of all of the above variables
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20
Q

What Does CO reflect

A

CO will reflect not only heart function but also the response of the circulatory system to both acute and chronic diseases as well as therapeutic interactions

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21
Q

Normal CO

A

4-6 L/min

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22
Q

Preload

A

In a normal heart it will be preload that will determine cardiac output

Frank-Starling increase preload dealt with an increased CO

In an abnormal heart when it cannot pump all the blood it receives then it is the hearts pumping ability that will determine CO

When we see JVD we can assume that the preload of the right heart has increased so that CVP has also increased

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23
Q

AFTERLOAD

A

In a healthy heart the afterload has minimal effect

A sudden increase in afterload will drop SV for a couple of beats, but then an increase in blood levels will cause an increased stretch and increased pumping, meaning that stroke volume is maintained

Increased afterload means that increased myocardial work and increased oxygen consumption

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24
Q

CONTRACTILITY

A

Ejection fraction is a measure of contractility

A heart with an increased contractility will produce a greater stroke volume for a given preload

Compared to another heart with the same preload and afterload

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25
Q

Frank Starling Law

A

The more that the heart is filled during diastole, the greater the subsequent force of contraction (increase in SV)

The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return

There is a point however where overstretch can be reached and CO will plateau and then begin to fall

The Y axis is the for of contraction= CO

In addition to the Frank-Starling mechanism increased stretch in the right atrium will also stretch the SA node which will increase the frequency of the impulse the SA node generates

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26
Q

The Frank Starling Relationship

A

The Frank Starling Relationship is the basis for

Matching CO to venous return

Balancing the output of right and left ventricles

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27
Q

Arterial Lines

A

A catheter is inserted into an artery and connected to a pressure transducing system

Reflects the afterload of the left ventricle

An important hemodynamic parameter as it is the best indicator of overall perfusion

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28
Q

Arterial Lines-Measuring

A

Allows for continuous monitoring of systemic blood pressure

Allows for assessing trends, responses to fluids and medications

Allows for continuous MAP monitoring

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29
Q

MAP

A

Average pressure in arteries during a cardiac cycle

MAP <60 mmHg indicates impaired tissue perfusion

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30
Q

Hypotension is a late sign of what?

A

Hypotension is a late sign of deficits in blood volume and/or cardiac function

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31
Q

MAP Equation

A

MAP =(Systolic x 2 diastolic) / 3

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32
Q

Systemic Vascular Resistance (SVR) Normal

A

1200-1600 dynes.sec.cm^ -5

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33
Q

Systemic Vascular Resistance (SVR) Equation

A

SVR=[(MAP-CVP)/CO] x 80

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34
Q

Systemic Vascular Resistance (SVR) Definition

A

Resistance to blood flow from all systemic vasculature

Not directly measured rather it is calucated

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35
Q

Systemic Vascular Resistance Index (SVRI) Normal

A

1600-2400 dynes.sec.cm^-5/m^2

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36
Q

Systemic Vascular Resistance Index (SVRI) Definition

A

SVR of that of the wall of the left ventricle during enjection

Not directy measured but rather a calculated measure

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37
Q

Central Venous Pressure

A

When a central line is connected to a pressure inducer system we can obtain the central venous pressure (CVP)

CVP can give an indication of right heart function and fluid balance

Reflects the preload on the right side of the heart

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38
Q

CVP Normal

A

CVP 2-8 mmHg

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39
Q

CVP numerical pressure value is a result of the following factors:

A
  • Right heart pumping capabilities “pump”
    • If R heart pumps the blood it receives, blood will not back up in R atrium and CVP should be normal
  • Venous tone determines venous vascular space “pipe”
    • More vascular space would mean a lower CVP, less blood is returning to the R heart
  • Blood volume “fluid”
    • Volume must be adequate to fill vascular space, decrease blood volume means lower CVP
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40
Q

Increases in CVP

A
  • Increased intrathoracic pressure
    • Positive pressure ventilation
    • Tension pneumothorax
  • Right heart failure
  • Hypervolemia
  • Compression around the heart
    • Cardiac tamponade
      • Severe asthma can cause a tamponade around the heart
    • Constrictive pericarditis
  • Technical
    • Misplaced transducer
      • Below the level of the right atrium
    • During infusion of fluid
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41
Q

Decreases in CVP

A
  • Hypovolemia
    • Dehydration
    • Blood loss
    • Third spacing
      • Loss of fluid in interstitial space
  • Vasodilation
    • Shock
    • Drugs
  • Spontaneous breathing
    • During inspiration
  • Technical
    • Misplace transducer
    • Above level of right atrium
    • Air bubbles in line
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42
Q

Pulmonary Vascular Resistance (PVR) Normals

A

120-240 dynes.sec.cm^-5

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43
Q

Pulmonary Vascular Resistance (PVR) Calculation

A

PVR=[(Mean PAP-PCWP)/CO] x 80

44
Q

Pulmonary Vascular Resistance Index (PVRI) Normal

A

200-400 dynes.sec/cm-5/m2

45
Q

Pulmonary Vascular Resistance Index (PVRI) Calculation

A

PVRI= [(MPAP-PAWP)/CI] x 80

46
Q

Pulmonary Vascular Resistance Index (PVRI) Definition

A

PVR based on a average body size

It is a calculated measure

47
Q

Pulmonary Artery Pressure (PAP) Normal

A

(20-30)/(6-15) mmHg

48
Q

Pulmonary Artery Pressure (PAP) Definition

A

Volume ejected by RV and resistance of flo thruogh pulmonary vasculature

Directly measured by measureed by pulmonary artery catheter

Measure of right heart afterload

49
Q

Mean Pulmonary Artery Pressure (mPAP) Normals

A

10-20 mmHg

50
Q

Mean Pulmonary Artery Pressure (mPAP) Definition

A

Average pulmonary pressure used to determine hypo/hypertension

It is a direct measure of pulmonay artery catheter

51
Q

Pulmonary wedge Pressure (PAWP) Normals

A

4-12

52
Q

Pulmonary wedge Pressure (PAWP) Desciption

A

Indirect measure of pressure in the left atrium

Direct measurement through the pulmonary catheter

Reflection of left heart preload

53
Q

Stroke Volume (SV) Normals

A

60-130 ml/beats

54
Q

Stroke Volume (SV) Equation

A

SV=CO/HR

55
Q

Stroke Volume (SV) Description

A

Volume of blood pumped out of the heart per beat

Calculated measure

56
Q

Stroke Volume Index (SVI) Normals

A

30-50 ml/min/m2

57
Q

Stroke Volume Index (SVI) Equation

A

SVI= SV/Body SA

58
Q

Stroke Volume Index (SVI) Description

A

SV in reference to body surface area and is a calculated measure

59
Q

Cardiac Index (CI) Normals

A

2.5-4 L/min/m2

60
Q

Cardiac Index (CI) Equation

A

CI=CO/Body SA

61
Q

Cardiac Index (CI) Description

A

Index of pt. body size to cardiac output and is a calculated measure

62
Q

Arterial Line-Verifying Function

A
  • Discrepancies between non-invasive measurements and invasive measurements are considered normal as long as the artline pressure is higher than the cuff pressure
    • Is the artline is lower than the manual the system is damped or the transducer is not levelled
  • Artlines should be zeroed (recalibrated) every 12 hours (Q12)
  • Levelling should also happened with each patient repositioning
63
Q

Arterial Line-Waveform

A

Inspecting Waveform

Should see a clear arterial pressure waveform with a dicrotic notch

If there is no dicrotic notch-May mean there is extreme hypotension (SBP < 50 mmHg)

May mean system is damped

64
Q

Blood Pressure “Normal”

A

BP usually fairly stable due to homeostatic mechanisms

Decreases in BP are a late sign of problems as the body usually compensates (maintains BP through increased SVR)

65
Q

Increased Blood Pressure

A

Increased SVR (for specific see Ÿ SVR)

Increased CO (Improved circulatory volume, improved circulatory function

66
Q

Decreases in Blood Pressure

A

Hypovolemia (fluid or blood loss)

Cardiac failure

Shock

Vasodilation (see SVR)

Transducer placed above level of RA if on artline

67
Q

Central Venous Pressure

A

Pressure of the blood in the right atrium and vena cava and right ventricle during diastole when the tricuspid valve is open and unobstructed

Usually in the jugular vein but sometimes is located in the subclaviamIn both cases will extend down to the vena cava or right atrium of the heart-The only exception is if it is inserted from the femoral

68
Q

VENTRICULAR PRELOAD ASSESSMENT

A
  • Atrial filling pressure approximates ventricular end-diastolic pressure (VEDP)
    • This is reflected by a in the diagram
  • There is a non linear relationship between VEDP reflecting VEDV when
    • No valvular disease
    • Normal ventricular wall compliance
  • CVP ~ RVEDP ~ RVEDV (preload)
69
Q

Jugular Venous Distention

A

Clinically CVP can also be estimated through Jugular Venous Distention JVD

Normal JVD is <3 cm above the sternal angle

Most common cause of JVD is right sided heart failure but may be secondary to left sided failure or chronic hypoxemia (pulmonary vasoconstriction)

70
Q

Assessment of JVD

A

Place the patient into a semi-folwers position @ 45°

If the patient hasn’t changed position much you can measure it form their position (more common measurement)

Measure at the end of exhalation

71
Q

INDICATION OF CENTRAL LINE

A
  • Need to monitor CVP
  • Need to access/administer
    • Large amounts of fluid/blood
    • Medications
      • Especially vascoactive or hyper/hypotonic medication
  • Pacemaker placement
    • Transvenous pacing
  • Poor peripheral access
  • Allows for blood smapling
72
Q

COMPLICATIONS OF CENTRAL LINE

A

Pain

Infection bleeding

Air embolism

Thrombosis and thromboembolism

Pneumothorax-Depending on site used

73
Q

Central Venous Pressure response to positive pressure ventilation and spontaneous breathn

A

Increased with positive pressure ventilation but decreased with spontaneous breathing

74
Q

neurogenic shock

A

All hemodynamic readings are low and there will be no increase in HR and SVR to compensate

75
Q

hypovolemic shock,

A

In hypovolemic shock, we see decreased volumes, meaning decreased pressures and CO in the heart, however HR and SVR will increase to compensate (unlike in neurogenic shock)

76
Q

septic shock,

A

In septic shock, patient’s are fluid resuscitated, meaning they will have lots of fluid on boarding, leading to an increased CO.

The SVR will be decreased in septic shock as the blood is pooling in the extremities and not returning to the heart, leading to decreased BP.

Therefore the HR will increase to compensate for the hypotension and lack of perfusion (even though there is lots of fluid)

HR and SVR are in a direct relationship and are compensatory measures (except for in septic and neurogenic shock). They will increase to compensate for decreased CO and decrease to compensate for increased CO.

77
Q

What measure do BP and MAP reflect

A

Blood pressure

Mean arterial pressure

78
Q

What does the ejection fraction reflect

A

Contractility of the heart

79
Q
A
80
Q

SvO2

A

Measured in the PA port

Some have continuous monitoring via reflection spectrophotometry

81
Q

Ca-vO2

A

Can assess for left to rt shunt by measuring from CVP (Proximal port) and PA distal

82
Q

Mixed venous sampling

A
  • Will get this sample from dital port of pulmonary artery catheter (only place you can get a true mixed venous smaple!
  • Mixed venous is getting blood from all the body including blood from heart and lungs
  • SvO2 and C(a-v)O2
83
Q

Pulmonary Artery Pressure and Respiration

A
  • PAWP should be measured when pleural pressure is near zero or close to zero
  • During mechanical PPV especially PEEP, PAWP can be overestimated from transmission of positive pressure to the catheter
  • PEEP < 10 cmH2O show limited effect on PAWP
  • The effect of PEEP on pleural pressures is enhanced with:
  • Increased lung compliance
  • Decreased thoracic compliance
84
Q

An Increase in PAP

A

1)Increased pulmonary blood flow

  • Volume overload
  • Left to right shunt (PDA)

2) Increased PVR

  • Pulmonary emobli, acute or chronic lung disease, cardiac tamponade, left heart failure
85
Q

Clinical Management of Preload

A

1) Increase Volume

I.V. infusion of fluid

end result is ­ preload, which will ¯ PVR/SVR and ¯ HR

2) Decrease Volume

Diuretics: serve primarily to ¯ preload by diuresis or reduction of intravascular volume.

end result is ↓ preload

86
Q

Clinical Management of Afterload

A

Afterload (Pipe)

Vasodilator Therapy: Use when SVR/PVR is high, vasodilators will alter the size of the vascular bed by direct relaxation of vascular smooth muscle

• end result is a decrease in SVR/PVR, afterload, and preload

Vasopressor Therapy: Use when SVR/PVR is low, vasopressors will cause peripheral vasoconstriction following stimulation of alpha receptors.

End result is­ an increase in afterload, ­ SVR/PVR, ­ preload

87
Q

Clinical Management of Contractility

A

Positive Inotrope: Force of myocardial contractility in an effort to improve ventricular performance. (C.O.). Be mindful of the increase in myocardial O2 consumption, as if not properly managed you run the risk of ischemia

Examples (dopamine, dobutamine, epinephrine, milrinone)

Negative Inotrope: ↓ force of myocardial contractility and O2 requirements of heart

Examples (calcium channel blockers, beta blockers)

88
Q

Hypovoluemic shock

A

Everything is decreased so HR and SVR are trying to compensate

89
Q

Cardiogenic Shock

A

Everythgin goes up but BP and CO

90
Q

Septoc Shock

A

Everything goes down

CO can go up or down

HR and SVR go up to compensate

91
Q

Neurogenic Shock

A

Everything absolutely go down

92
Q

Obstructive Shock

A

CVP goes up

PAP and PAWP can go up or down

BP and CO go down

HR and SVR go up

93
Q

Invasive CO MEasurement

A

Thermodilution (see how long for the cold to dilute so a longer curve equal lower CO)

Dye Dilution (see how long so the dye to absorb)

Fick Method (Estimation, but considered to be the gold standard)

94
Q

CO Measurement Non-Invasive

A

Echocardiograph

TEE

95
Q

Arterial O2 Content (CaO2)

A

Total amount of oxygen contained in arterial blood; going to the body

Oxygen is carried by

  • Hemoglobin (Hb)-major carrier of O2
  • Dissolved in Plasma

CaO2 = (Hb x 1.34 ml/g) * SaO2 + (PaO2 x 0.003 ml/100ml/mmHg)

96
Q

Mixed Venous O2 Saturation (SvO2)

A

Saturation of the blood in the pulmonary artery

True mixed venous blood is in the pulmonary artery

The sample is drawn from the distal port of the PA catheter and analyzed on the blood gas machine

Some specialized PACs measure SvO2 continuously, in vivo

An early indicator of changes in O2 transport status

97
Q

Increased SVO2

A
  • Increased CO
  • Decreased O2 consumption
  • Skeletal muscle relaxation
  • Certain Poisons
  • Peripheral shunting
  • hypothermia
98
Q

Factors that Decrease SvO2

A
  • Decreased CO
  • Anemia
  • Decreased SaO2
  • Increased O2 Consumption
  • Exercise
  • Hyperthermia
  • Increase metabolic rate
99
Q

•Mixed Venous O2 Content (CvO2)

A

CvO2 = (Hb x 1.34 ml/g) * SvO2 + (PvO2 x 0.003 ml/100ml/mmHg)

Normal = 13 - 16 mL/dL (vol%)

100
Q

•End-capillary O2 Content

A
  • Ideal amount of oxygen contained in the blood of the pulmonary capillaries
  • Used when calculating shunt

CcO2 = (Hb x 1.34 ml/g) * ScO2+ (PAO2 x 0.003 ml/100ml/mmHg)

Normal < 10 %

101
Q

•Oxygen Delivery (DO2)

A

Total oxygen delivered to body

  • Requires:
  • Arterial O2 content
  • Cardiac Output (C.O.) or (QT)

DO2 = QT * (CaO2 * 10)

102
Q

Factors that Decrease C(a-v)O2 (and decrease VO2)

A
  • Increased C.O.
  • Skeletal muscle relaxation (drugs)
  • Peripheral shunting (sepsis or trauma)
  • Certain Poisons (cyanide)
  • Hypothermia
103
Q

Factors that Increase C(a-v)O2 (and \ increase VO2)

A
  • Decreased C.O.
  • Increased O2 consumption
  • Exercise
  • Shivering
  • Hyperthermia
  • Seizures
104
Q

Factors that Increase O2ER

A
  • Decreased C.O.
  • Increased O2 Consumption
  • Anemia
  • Decreased arterial oxygenation
105
Q

Factors that Decrease O2ER

A

•Increased C.O.
•Peripheral shunting
•Certain poisons
•Hypothermia
•Increased hemoglobin
•Increased arterial oxygenation
•

106
Q

Shunt Fraction

A

<10%-Normal

10-19%-Seldom need vent support

20-29%Require PEEP or CPAP

30 or more- life threatening need mechanical vent with PEEP

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