Table of contents
- 1. Introduction
- 2. Pressures
- 2.1. LV Pressures
- 2.2. Wedge
- 2.3. PA Pressures
- 2.4. RV Pressures
- 2.5. RA Pressures
- 3. Aortic Pressure
- 4. Cardiac Output
- 4.1. Thermodilution
- 4.2. Fick Method
- 5. Normal Values
- 6. Setup
- 7. Specific Situations
- 8. Formulas
.
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%)
- AV O2 difference = Hb (g/L) * 1.36 * [% Art Sat - %Mixed Venous Sat]
- 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)
- Can measure in 3 ways:
- 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)
- With each measurement, pt must be positioned so that the transducer is at the mid-AP-level
- 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 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 decreased4 Further elevation of intrapericardial pressure, lowers RA and
wedge pressuresWorsening 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
- X descent is prominent
- 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
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 pericardiumPA 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) - 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.
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 = O2 consumption / AV difference in O2 content
- Fick Method
- Advantages:
- Better for lower CO measurements
- Disadvantages
- Can be inaccurate b/c don't have a CO2 hood
- Advantages:
- Thermodilution
- Advantages:
- Better for higher CO
- Disadvantages:
- Worse if shunt, TR, low CO
- Advantages:
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