Hemodynamics

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    Introduction

    • All pressure measurements recorded with respect to atmosphere (in mmHg)
    • Pressure within chamber - Intrathoracic Pressure = transmural pressure
    • All pressure measurements are the SUM of INTRACARDIAC and INTRATHORACIC measurements
      • Often intrathoracic pressure is ignored b/c it's too small (but higher in lung disease and distress)
      • Intrathoracic pressure measured in cmH2O
      • cmH2O * 0.74 = mmHg
      • Can estimate intrathoracic pressure via esophageal probe (but often not needed)

     

    Pressures

    LV Pressures

    • LV systolic = aortic systolic (if no LVOT obstruction)
    • LV end-diastolic = Wedge (if no mitral valve disease)
      • End-diastole = QRS onset on ECG
        • Important!!
        • Because represents LV filling pressure
        • Diseased myocardium = higher pressure needed to maintain filling volume
      • Optimal pressures = 3-12
      • In diseased myocardium optimal filling pressures can go up to 20-25mmHg, at the expense of pulmonary congestion.

     

    Wedge

    • Represents INDIRECT LA pressure
    • Wedge pressure = dampened due to long transmission through pulmonary vascular ped
    • See A and V waves that are dampened, and C wave is usually absent due to dampening
      • A delay (to ECG recording) is also introduced due to retrograde transmission
    • Normal Wedge = 2-12mmHg
      • Twice that of RA pressure
    •  
    • Waves
      • A-wave

        LA systolie (follows P-wave by 200ms)

        • Increased Mitral Stenosis
        • Increased in LV non-compliance
        C-wave

        Closure of mitral valve + LV systole onset

        • Seen in LA recording
        • NOT SEEN in wedge pressure due to dampening
        V-wave

        Venous filling after mitral valve closure.  Peak = end of LV systole

        • V-wave can be dominant in normal patients
        • Increased V-wave in MR
        • Increased in VSD
        X-descent

        LA Relaxation + downward motion of AV junction in LV systole

        • Decreased in MR
        Y-descent

        LA emptying into LV (marks onset of LV diastole)

        • Decreased in MS
    • IMPORTANT!!  LA V-wave vs. PA S-Wave
      • Peak of V-wave occurs AFTER T-wave of ECG
      • Peak of S-wave (PA) occurs close to the same time as T-wave on ECG
      • **V-waves comes LATER than PA systole (important to distinguish from PA in pts with giant V-wave)**
    • Clinically, Wedge can be used to:
      • Optimize LV filling pressure (volume or diuretics)
      • Estimate pressure in PA vascular bed
      • Normal Values:
      •   Normal LV Damaged LV
        Normal Wedge 2-12 15-20
        Optimal Wedge 15-20 20-25

        Pulmonary Edema

        (if albumin not low)

        25 mmHg

        30 mmHg

        (increased lung
        lymphatic drainage)

      • Cardiogenic pulmonary edema can occur in minutes (single myocardial ischemia can instantaneously raise wedge to 40), but takes days to resolve.
      • Cannot measure wedge for long period of time (balloon damage PA artery), but can trend PA-diastolic, which correlates well. 
      • LA kick is necessary to raise LV end-diastolic pressure (LVEDP) without raising pulmonary pressures
    • Wedge is inaccurate estimation of LVEDP in:
      • Mitral Stenosis - Overestimates LVEDP
      • Mitral Regurg + large V-wave - Overestimates LVEDP
      • Noncompliant LV (acute MI) - Underestimates LVEDP
    • Wedge measurement is simply inaccurate when:
      • Abnormal pulmonary vascular bed (lung disease or PE)
      • High intrathoracic pressure cause pulmonary vascular bed collapse
        • (Parenchymal lung disease)
      • Low LA pressure resulting in collapse of pulmonary capillaries
        • (volume depletion)
      • Location of catheter in poorly perfused area of lung
    • Rules:
      • A and V-waves must be visible (means communcation to LA)
      • Wedge must always be lower than PAd (otherwise bloodflow would reverse
    • Wedge is very sensitive to intrathoracic pressures
      • Elevated intrathoracic pressure for any cause = blocks retrograde transmission to catheter tip by collapsing alveolar capillaries.
      • A and V-waves must be seen
        • If they are not seen, wedge is in Zones 1 and 2 of the lung, where alveolar pressure is higher than pulmonary venous pressure, causing collapse, and you are measuring alveolar pessure.
        • All measurements must be measured End-Expiration (when intrathoracic pressure is close to zero)
        • Lung disease change intrathoracic pressure, and make wedge not reliable
      • PEEP (esp >10 cmH2O) can raise intracardiac pressure
        • --> can collapse capillaries and pulmonary veins --> loss of AV waves poor estimation
        • --> can cause significant variation and over-estimation at end-expiration.

    PA Pressures

    • Waves
      • S-wave

        (Systole)

        PA systole

        • Coincides with T-wave on ECG

        N

        (Dicrotic Notch)

        Pulmonic Valve Closure

        D

        (Diastole)

        Diastolic Pressure

        • Within 5mm of wedge
          (if normal pulmonary vascular resistance)
    • Peak of PA systolic pressure = onset of QRS
    • Dicrotic notch = pulmonary valve closure (end of RV systole)
    • Peak of PA systole comes earlier than wedge V-wave
    • PA end-diastole = mean Wedge = LVEDP  EXCEPT when:
      • Abnormal pulmonary vascular bed (increased resistance) - overestimates
      • MR with larve V-wave - underestimates

     

    RV Pressures

    • Normals:
      • Systolic: 15-30
      • End-Diastolic: 2-8
    • If no RV port, use RA pressure to estimate RVEDP
    • No need to monitor RV pressure continuously

     

    RA Pressures

    • Waves
      • A-wave

        Atrial contraction

        • Higher if non-compliant RV
        • Peak follows ECG P-wave by 80ms
          (electromechanical delay + transduction delay)
        C-wave

        Tricuspid Valve closure + RA systole onset

        (minor wave, but can be usually seen)

        • Onset at start of QRS complex
        • RA systole
        • Associated A-wave by PR interval (seen better with high PR)
        V-wave

        Venous filling, closed Tricuspid valve

        • Peaks at end of RV Systole
        • Occurs during T-wave
        • Increased in RA overload + TR
        X-descent

        RA relaxation + downward motion of AV junction during RV systole

        • Decreased in TR
        • C-wave interrupts X-descent, X-descent after C-wave is X'
        Y-descent Rapid exit of blood from RA to RV
    • RA pressure = RVEDP (if no TS or TR)
    • If heart is normal, RA pressure can predict LA pressure.

     

     

     

    Aortic Pressure

    • Normas:
      • Systolic: 100-140
      • Diastolic: 60-90
      • Mean: 70-105
    • 5-10mm Lower during inspiration
    • Dicrotic notch = Aortic valve closure = end of LV systole
    • Timing with ECG is not consistent (depends on how close catheter is to Aortic Valve)
      • The more peripheral you go, systolic pressure rises, diastolic + mean decrease.
      • Dicrotic notch lowers, the more peripheral you go
      • During vasoconstriction, peripheral sBP < central sBP

     

    Cardiac Output

    • Expressed Liters/min
    • Cardiac index = CO / BSA
    • Normal Index: 2.6 - 4.2 L/min/m^2
    • Important to measure stroke volume!!! (b/c heart rate changes can affect CI)
      • SVI = SV / BSA
      • Normal SVI: 30-64 mL/beat/m^2
    • Two methods to measure:
      • Thermodilution
      • Fick Method
    • Usually Pulmonary Flow = Systemic Flow (unless LV regurgitation - AR or MR)
    • SVR = (MAP - RAP)*80 / CO    [80 = wood to dynes conversion]
      • Normal SVR = 700-1600 dynes-sec-cm^-5

     

    Thermodilution

    • Measures pumonary blood flow (= systemic blood flow unless L-R shunt exists)
    • Introduced by Fegler in 1954 (Ganz refined it in 1971)
    • Cold solution (indicator) injected into RA through proximal port of PA catheter
    • Thermister detects temperature change in PA and plots °C vs. time (s)
    • Curve = smooth upstroke + slow decline to baseline
    • Area under the curve measured  --> Stewart-Hamilton equation to yield CO
    • In the old days used ice temperature in a bucket, but recent literature said room temperature is just as accurate.
    • To have good measurements:
      • Proper computation constant (by catheter manufacturer based on temperature of injectate, volume, catheter)
      • Inject precise volume (10mL) over 2-4s
      • Ensure no rhythm or rate change during measurement
      • If using ice - do not allow to warm before injecting. (inject in 15s)
      • Measurements should be within 10% (first one usually most different - catheter is cooled in first injection)
      • Examine curve!!!
        • TR invalidates the curve --> see slow decay to baseline

     

    Fick Method

    • Developed by Adolph Fick (1870)
    • Cardiac output = O2 consumption (mL of O2/min) / AV difference (in mL of O2/L of blood)
    • AV O2 difference is important!!
      • Measure Hemoglobin, arterial O2 sat, mixed venous sat
      • Mixed venous = PA sample  (distal lumen of PA catheter)
      • Assume RBCs with 100% sat = 1.36 mL of O2 / gram of Hb
      • Arterial O2 content = Hb (g/dL) *10 (dL to L) * 1.36 (mL O2/g of Hb) * O2sat(%) = mL of O2/L of blood
      • Simplify to:
        • AV O2 difference = Hb (g/L) * 1.36 * [% Art Sat - %Mixed Venous Sat]
          • May need to convert g/dL to g/L
          • Use decimals for % (i.e. 0.25 instead of 25%)
    • O2 Consumption is important!!!
      • Can measure in 3 ways:
        • Collect exhaled air using hood (not practical)
        • Analyze inhaled and exhaled O2 content + metabolic charts  - using indirect calorimetry
        • Assumed as basal 125mL O2/min/m^2  (but ICU pts an consume more O2, so can be inaccurate)
    • Sources of error:
      • Incorrect sat measurements (withdraw 2-3mL and discart before measuring)
      • Peripheral shunting (septic shock - PA can have high O2 content despite poor CO)
      • Mitral/Aortic Regurg  (misses regurgitant volume output)
      • Intracardiac shunt (pulmonary flow DO NOT equal systemic flow)

    Normal Values

    • LV Pressure

      Systolic 100-140

      End-Diastolic 3-12

       
      Wedge

      2-12mmHg - Normal LV

      10-15mmHg - Diseased LV

       
      RV Pressure

      Systolic: 15-30 mmHg

      Diastolic: 2-8 mmHg

       
      PA

      Systolic: 15-30

      Diastolic: 4-12

      Mean: 9-18 (normal=15)

       
      Cardiac Index (CI) 2.6-4.2 L/min/m^2  

      Stroke Volume Index

      (SVI)

      30-64 mL/beat/m^2 Measured to avoid HR influence on CI
      SVR 700-1600 dynes-sec-cm^-5 SVR = (MAP-RAP)*80 / CO

      Total Pulmonary Res.

      (TPR)

      100-300 dynes-sec-cm^-5 TPR = mPAP *80 / CO

      Pulmonary Vascular Res

      (PVR)

      20-130 dynes-sec-cm^-5 PVR = (mPAP - mPCWP)*80 / CO

     

    Setup

    • Swan-Ganz Catheter
      • Usually 8.5Fr (usually needs that sheath size)
      • Has Ports:
        • Temp sensor
        • Distal pressure channel
        • Proximal Pressure Channel
        • (RV Pressure Channel -optional, can also use to feed pacer wire)
        • (Fiber optic continuous PA sat measurement - optional)
        • RA Pressure Channel
    • Pressure Transducer outside the body (converts mechanical to electrical signals)
      • Non-compliant tubing connection to transducer 
      • Keep length to a minimum
      • Minimize stop-cocks
    • Transducer contains a thin diaphragm - generates electrical signals when moves
      • Must be zeroed and calibrated
      • Transducer has a stopcock to expose line to atmosphere to set the atmospheric zero-reference point.
      • All pressures compared to atmosphere
      • Zero-reference must set at the level of the heart (halfway between AP diameter)
        • With each measurement, pt must be positioned so that the transducer is at the mid-AP-level
          (assumed location of the heart)
    • Insertion
      • Fluoro is not needed usually b/c each chamber has characteristic flow
      • Can use distance markers to help:
        • SVC 10-15cm

          - Inflate ballon a this point

          - If seeing respiratory variation - confirms intrathoracic

          RA 15-20cm  
          RV 30-40cm  
          PA 45-55cm  
          Wedge 45-60cm If greater - consider coiling somewhere
      • Confirm position on a post-Xray

     

     

    Specific Situations

    Respiratory Distress

    • If wedge alters by 10-15mmHg with respiratory variation, End-Expiratory wedge is likely overestimation.
      • If you can measure intrathoracic pressure, you can subtract from all pressures.  (use intra-esophageal pressure)
      • Attempt to quiet breathing
      • Attempt to get patient to drink through a straw
      • Attempt to sedate or paralyze (if you can)

     

    Mechanical Ventilation

    • During inspiration: Intrathoracic pressure is increased, venous return is decreased (opposite) 
    • Still measure at end-expiration
    • Often must paralyze or sedate to get proper measurement.
    • PEEP
      • Can be deliberately applied by vent OR gas-trapping causing auto-peep
      • If PEEP < 10 - effect is small
      • If PEEP > 10 - effect is large!!
        • Degree of PEEP transmission to cardiac pressure varies (cannot subtract!!)
        • Not advised to discontinue PEEP (can worsen cardiac status and hypoxemia)
          • Hemodynamics can be completely different!
        • NO SOLUTION
          • Use clinical sense -- if oliguric, can try volume challenge and see how wedge and hypoxemia change. 
      •  

     

    Pericardial Tamponade

    • Classically:
      • ​Hypotension
      • Pulsus paradoxus
      • Equilization of intracardiac pressures
    • Kussmaul's sign not seen in pericardial tamponade!! (shouldn't be seen) - common misconception
      • In constrictive pericarditis it is seen b/c scarred pericardium blocks transmission of negative thoracic pressure to RA, but in tamponade there is fluid there to transmit the pressure. 
    • Pulsus Paradoxus
      • Normal BP drop between inspiration/expiration
      • >10mm = significant (arbitrary)
      • Seen in pts with lung disease and shock
      • In tamponade, there is arterial systolic variation (not diastolic)
      • It is not a "paradox" because it's exaggeration of normal physiology
        • "Paradox" came from auscultation of normal heart sounds, but intermittently no palpable pulse.
      • Pulsus paradoxus can be absent in pts with LV dysfunction (unclear why)
    • ​Stages:
    1. 1

      Intrapericardial pressure LESS than RA and  LESS than Wedge

      Not much change
      2

      Intrapericardial pressure MORE than RA but LESS than Wedge

      RV tamponade --> strokeIntra volume comromized
      3 Intrapericardial pressure MORE than RA and MORE than Wedge

      R + L heart fluid compression exists

      Pericardial pressure = RA pressure = LA pressure

      Pulsus paradoxus magnified + stroke vol
         significantly decreased

      4 Further elevation of intrapericardial pressure, lowers RA and
         wedge pressures
      Worsening stroke volume ---> shock --> death
    • RA Pressure Findings
      • X descent is prominent
        • During systole, intrapericardial pressure falls, RA pressure also falls causing a steep X descent
      • Y descent is attenuated or gone ("Lose your Y before you die")
        • During diastole, blood from RA goes to RV, but intrapericardial pressure doesn't change (total cardiac volume is the same!).
        • As such, Y descent does not occur
    • Doc - Sep 19 2017 - 11-32 AM - p1.jpg

    • Stroke volume measurement is CRUCIAL!
      • Compensatory tachycardia can raise CO and CI
    • Constriction vs. Tamponade
      • Construction has Kussmaul's Sign!
      • Constriction has prominent Y descent!

     

    Pericardial Constriction

    • Infection, inflammation, or malignancy can cause pericardium to be thickened, scarred, or non-compliant
    • Diastolic volume of heart reduced and atrial+ventricular filling pressures are elevated
    • ALL cardiac chambers involved equally (unlike restrictive cardiomyopathy)
      • Pulsus Paradoxus in 1/3 of Pericardial Constriction (compared to ~100% of tamponade)
    • Hemodynamic findings:
      • RA and Wedge are significantly elevated!

          12-15mmHg = moderate constriction

          20-25mmHg = severe constriction

         

        RA and LA pressures are nearly identical

        (Unless there is MR/TR, which can modify them)

        Exaggerated Y descent

        Sudden ventricular filling in early diastole
        Steep X descent Atrial volume ejected into RV, transiently reducing constriction

        RA pressure characteristic W or M pattern

        (due to steep Y and X descents)

        - If AFib --> A wave is gone

        - Y>X descent usually

        constriction.jpg

        NO change in RA pressure with inspiration

        IF SEVERE --> RA pressure increases

        with inspiration (Kussmaul's sign)

        Stiff non-compliant pericardium prevents transmission of
        negative inspiratory pressure in pericardium

        PA pressure elevated (35-40mmHg)  

     

    Effusive-Constrictive

    • Causes
      • TB, Mediastinal Radiation, Uremia, Malignancy (pericardial)
    • Tamponade findings predominant until effusion is removed
    • After removal of effusion --> constriction becomes apparent

     

    Restrictive Cardiomyopathy

    • Myocardial relaxation is restricted --> hemodynamics resemble pericardial constriction
    • Causes
      • Hemochromatosis, endomyocardial fibrosis, amyloidosis, myocarditis
    • Hemodynamics
    • RA and Wedge pressures are elevated (15-25mmHg)  
      Prominent X and Y descents (X=Y or Y>X)  
      ***RA and Wedge are usually not equal***  

      RA and LV filling pressures are elevated but NOT equal

      LA ≠ RA pressure

       
      ***Higher pulmonary pressures (>50 mmHg)  
      *** = contrast restriction vs constriction
    • Pulsus paradoxus may be present (but uncommon)
    • Sometimes impossible to tell constriction vs. restriction --> use US, MRI, CT
      • IF still cannot tell apart, sometimes explorative thoracotomy is used to examine pericardium.

     

    Tamponade vs. Constriction vs. Restriction

    • comparison.jpg

    Formulas

    • V = IR
    • [Mean Pressure Difference] = FLOW * Resistance
    • Dynes = Wood Units * 80

     

    Pulmonary Vascular Resistance

    • Calculated:
      • mPAP - PCWP / Flow = Resistance in WOOD UNITS
      • Convert Wood Units to Dynes x 80
      • Pulmonary Hypertension > 2.5 Wood Units
        • Mild-to-Mod: 2.5 - 5.0 Wood Units
        • Severe: > 5.0 Wood Units

     

    Systemic Vascular Resistance

    • Calculated
      • MAP - mRAP / Flow = Resistance in WOOD Units
      • Convert Wood Units to Dynes x 80
      •  

     

    Cardiac Index

    • Two ways to measure:
      • Fick Method = O2 consumption / AV difference in O2 content
        • O2 content = 
        • O2 consumption measured with a hood over head
          • Can estimate 125 * BSA
      • Fick = 125 * BSA / (1.36*Hb*[ArtSat - MixedVenSat]) 
    • Fick Method
      • Advantages:
        • Better for lower CO measurements
      • Disadvantages
        • Can be inaccurate b/c don't have a CO2 hood
    • Thermodilution
      • Advantages:
        • Better for higher CO
      • Disadvantages:
        • Worse if shunt, TR, low CO
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