Hemodynamics

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.

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)

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

• 

• 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 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

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