Hemodynamics Flashcards
Hemodynamics Definition
Study of forces and pressures that influence circulation of the blood
Main Routes to collect Hemodynamic Information
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
Liquids
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
Pascal Principals
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
Applying Pascal’s Principle-Blood Pressure
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.)
The Heart As Two Pumps
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
Applying Pascal’s Principle-Arterial Lines
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
Ohms Law-Electrical
Voltage = Current X Resistance
Ohms Law-Fluids
Pressure = Flow X Resistance
P= Driving Pressure
Resistance in the Left Heart Equation (Delta P)
Resistance = Delta P / Flow
P= BP =SVR X CO
P= Driving Pressure of the left side of the heart
CO=flow
Systemic Vascular Resistance-Equation
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)
FACTORS THAT INCREASE SVR
- Lt heart failure:
- CHF, cardio, hypovolemic & obstructive shocks
- Vasoconstricting Agents
- Examples: Dopamine, Epinephrine, Norepinephrine (Levophed)
- Hypovolemia
- Septic shock (late stages)
- Decreased PaCO2
FACTORS THAT DECREASE SVR
- Neurogenic shock
- Vasodilating agents
- Ex. Nitroglycerin, Morphine
- Septic Shock (early stages)
- Spinal shock
- PaCO2
PVR-Equation
PVR= ((MPAP-PAWP)/CO) x 80
According to this formula the driving pressure is MPAP minus PAWP.
FACTORS THAT INCREASE PVR
- Right-Sided Heart Failure:
- Pulmonary hypertension
- Pulmonary embolism
- Decreased
- Alveolar oxygenation
- Hypoxemia will cause pulmonary vasoconstriction
- pH
- Acidosis
- PaCO2
- Alveolar oxygenation
- 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
FACTORS THAT DECREASE PVR
- 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
Cardiac Output Definition
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
Cardiac Output Equation
CO= (HR x SV)
What is cardiac output determined by
- 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
What Does CO reflect
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
Normal CO
4-6 L/min
Preload
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
AFTERLOAD
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
CONTRACTILITY
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
Frank Starling Law
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
The Frank Starling Relationship
The Frank Starling Relationship is the basis for
Matching CO to venous return
Balancing the output of right and left ventricles
Arterial Lines
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
Arterial Lines-Measuring
Allows for continuous monitoring of systemic blood pressure
Allows for assessing trends, responses to fluids and medications
Allows for continuous MAP monitoring
MAP
Average pressure in arteries during a cardiac cycle
MAP <60 mmHg indicates impaired tissue perfusion
Hypotension is a late sign of what?
Hypotension is a late sign of deficits in blood volume and/or cardiac function
MAP Equation
MAP =(Systolic x 2 diastolic) / 3
Systemic Vascular Resistance (SVR) Normal
1200-1600 dynes.sec.cm^ -5
Systemic Vascular Resistance (SVR) Equation
SVR=[(MAP-CVP)/CO] x 80
Systemic Vascular Resistance (SVR) Definition
Resistance to blood flow from all systemic vasculature
Not directly measured rather it is calucated
Systemic Vascular Resistance Index (SVRI) Normal
1600-2400 dynes.sec.cm^-5/m^2
Systemic Vascular Resistance Index (SVRI) Definition
SVR of that of the wall of the left ventricle during enjection
Not directy measured but rather a calculated measure
Central Venous Pressure
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
CVP Normal
CVP 2-8 mmHg
CVP numerical pressure value is a result of the following factors:
-
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
Increases in CVP
-
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
- Cardiac tamponade
-
Technical
- Misplaced transducer
- Below the level of the right atrium
- During infusion of fluid
- Misplaced transducer
Decreases in CVP
- 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
Pulmonary Vascular Resistance (PVR) Normals
120-240 dynes.sec.cm^-5
Pulmonary Vascular Resistance (PVR) Calculation
PVR=[(Mean PAP-PCWP)/CO] x 80
Pulmonary Vascular Resistance Index (PVRI) Normal
200-400 dynes.sec/cm-5/m2
Pulmonary Vascular Resistance Index (PVRI) Calculation
PVRI= [(MPAP-PAWP)/CI] x 80
Pulmonary Vascular Resistance Index (PVRI) Definition
PVR based on a average body size
It is a calculated measure
Pulmonary Artery Pressure (PAP) Normal
(20-30)/(6-15) mmHg
Pulmonary Artery Pressure (PAP) Definition
Volume ejected by RV and resistance of flo thruogh pulmonary vasculature
Directly measured by measureed by pulmonary artery catheter
Measure of right heart afterload
Mean Pulmonary Artery Pressure (mPAP) Normals
10-20 mmHg
Mean Pulmonary Artery Pressure (mPAP) Definition
Average pulmonary pressure used to determine hypo/hypertension
It is a direct measure of pulmonay artery catheter
Pulmonary wedge Pressure (PAWP) Normals
4-12
Pulmonary wedge Pressure (PAWP) Desciption
Indirect measure of pressure in the left atrium
Direct measurement through the pulmonary catheter
Reflection of left heart preload
Stroke Volume (SV) Normals
60-130 ml/beats
Stroke Volume (SV) Equation
SV=CO/HR
Stroke Volume (SV) Description
Volume of blood pumped out of the heart per beat
Calculated measure
Stroke Volume Index (SVI) Normals
30-50 ml/min/m2
Stroke Volume Index (SVI) Equation
SVI= SV/Body SA
Stroke Volume Index (SVI) Description
SV in reference to body surface area and is a calculated measure
Cardiac Index (CI) Normals
2.5-4 L/min/m2
Cardiac Index (CI) Equation
CI=CO/Body SA
Cardiac Index (CI) Description
Index of pt. body size to cardiac output and is a calculated measure
Arterial Line-Verifying Function
- 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
Arterial Line-Waveform
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
Blood Pressure “Normal”
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)
Increased Blood Pressure
Increased SVR (for specific see SVR)
Increased CO (Improved circulatory volume, improved circulatory function
Decreases in Blood Pressure
Hypovolemia (fluid or blood loss)
Cardiac failure
Shock
Vasodilation (see SVR)
Transducer placed above level of RA if on artline
Central Venous Pressure
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
VENTRICULAR PRELOAD ASSESSMENT
- 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)
Jugular Venous Distention
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)
Assessment of JVD
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
INDICATION OF CENTRAL LINE
- 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
COMPLICATIONS OF CENTRAL LINE
Pain
Infection bleeding
Air embolism
Thrombosis and thromboembolism
Pneumothorax-Depending on site used
Central Venous Pressure response to positive pressure ventilation and spontaneous breathn
Increased with positive pressure ventilation but decreased with spontaneous breathing
neurogenic shock
All hemodynamic readings are low and there will be no increase in HR and SVR to compensate
hypovolemic shock,
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)
septic shock,
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.
What measure do BP and MAP reflect
Blood pressure
Mean arterial pressure
What does the ejection fraction reflect
Contractility of the heart
SvO2
Measured in the PA port
Some have continuous monitoring via reflection spectrophotometry
Ca-vO2
Can assess for left to rt shunt by measuring from CVP (Proximal port) and PA distal
Mixed venous sampling
- 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
Pulmonary Artery Pressure and Respiration
- 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
An Increase in PAP
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
Clinical Management of Preload
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
Clinical Management of Afterload
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
Clinical Management of Contractility
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)
Hypovoluemic shock
Everything is decreased so HR and SVR are trying to compensate
Cardiogenic Shock
Everythgin goes up but BP and CO
Septoc Shock
Everything goes down
CO can go up or down
HR and SVR go up to compensate
Neurogenic Shock
Everything absolutely go down
Obstructive Shock
CVP goes up
PAP and PAWP can go up or down
BP and CO go down
HR and SVR go up
Invasive CO MEasurement
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)
CO Measurement Non-Invasive
Echocardiograph
TEE
Arterial O2 Content (CaO2)
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)
Mixed Venous O2 Saturation (SvO2)
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
Increased SVO2
- Increased CO
- Decreased O2 consumption
- Skeletal muscle relaxation
- Certain Poisons
- Peripheral shunting
- hypothermia
Factors that Decrease SvO2
- Decreased CO
- Anemia
- Decreased SaO2
- Increased O2 Consumption
- Exercise
- Hyperthermia
- Increase metabolic rate
•Mixed Venous O2 Content (CvO2)
CvO2 = (Hb x 1.34 ml/g) * SvO2 + (PvO2 x 0.003 ml/100ml/mmHg)
Normal = 13 - 16 mL/dL (vol%)
•End-capillary O2 Content
- 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 %
•Oxygen Delivery (DO2)
Total oxygen delivered to body
- Requires:
- Arterial O2 content
- Cardiac Output (C.O.) or (QT)
DO2 = QT * (CaO2 * 10)
Factors that Decrease C(a-v)O2 (and decrease VO2)
- Increased C.O.
- Skeletal muscle relaxation (drugs)
- Peripheral shunting (sepsis or trauma)
- Certain Poisons (cyanide)
- Hypothermia
Factors that Increase C(a-v)O2 (and \ increase VO2)
- Decreased C.O.
- Increased O2 consumption
- Exercise
- Shivering
- Hyperthermia
- Seizures
Factors that Increase O2ER
- Decreased C.O.
- Increased O2 Consumption
- Anemia
- Decreased arterial oxygenation
Factors that Decrease O2ER
•Increased C.O.
•Peripheral shunting
•Certain poisons
•Hypothermia
•Increased hemoglobin
•Increased arterial oxygenation
•
Shunt Fraction
<10%-Normal
10-19%-Seldom need vent support
20-29%Require PEEP or CPAP
30 or more- life threatening need mechanical vent with PEEP
