Hemodynamics monitoring

Preload markers (static)

Most of them are useless for predicting fluid response. These measure “pressure,” not "flow."

Good for diagnosis, not for fluid decisions.

1. CVP

2. PAOP (pulmonary artery occlusion pressure)

3. IVC diameter & collapsibility (USG)

4. LVEDA (LV end-diastolic area on echo)

Preload markers (dynamic)

These predict whether a fluid bolus will increase stroke volume

1. Passive leg raise (PLR) test

2. Stroke volume variation (SVV) / Pulse pressure variation (PPV)

3. ΔVpeak (Aortic VTI variation)

4. End-expiratory occlusion test (EEOT)

Flow monitors

The most honest tools — measure stroke volume & CO

1. Echocardiography (VTI, LVOT diameter); Real-time cardiac output, SV, LV/RV function.

2. Swan–Ganz (PAC); Gold standard in complex cardiac, severe pulmonary HTN, RV failure.

Measures:

• CO (thermodilution)

• PA pressures

• PAOP

• SvO₂ (mixed venous O₂)

Tissue perfusion markers

• Lactate

• CRT

• Skin temperature

• ScvO₂ / SvO₂

ScvO₂ < 70% → extraction is high → delivery is low

Useful for titrating DO₂, especially in septic shock.

Respiratory-Circulation interaction tool

To check whether the heart is struggling with the lungs

• RV strain on echo: Helps detect RV failure from PEEP, pressure, or overload.

• VExUS (venous excess ultrasound): Hepatic vein, portal vein, IVC patterns show venous congestion. -> Strong predictor of kidney injury.

• IVC + hepatic vein Doppler: Venous pressure overload.

Renal perfusion tools

• Renal resistive index (RRI): High (>0.75) = poor renal perfusion.

• Doppler of renal segmental arteries: Flow-related AKI insights.

CVP

CVP reflects right-sided filling pressure.

If it is high, it means:

• The right atrium is already under pressure

• Venous return is congested

• The tank is not empty

• A hypovolemic patient cannot maintain a high CVP unless something else is wrong

• Low urine output with a high CVP = kidneys are congested. When the right atrial pressure is high, it back-transmits: → high renal vein pressure → increases interstitial pressure in the kidney → collapses tubular lumen → ↓ GFR → ↓ urine output. This is congestive renal failure, not volume loss. GFR depends on perfusion pressure (MAP – renal vein pressure) => Renal perfusion pressure (RPP) = MAP – CVP (renal venous pressure). If CVP is high, effective filtration pressure drops. 

Even if MAP is normal, if CVP is high: RPP falls -> GFR collapses -> Urine output falls. So this is congestion-induced AKI, not a dry kidney.

True hypovolemia should give:

• low CVP

• low JVP

• flat IVC

• A good urine output after small bolus

If the CVP is high, hypovolemia is ruled out unless there is :

• tension pneumothorax

• tamponade

• massive PE

• mechanically ventilated with high PEEP

• cor pulmonale

• RV failure

(In these cases, CVP is high but forward flow is poor → still not “volume responsive.”)

The kidney cares about flow, not CVP

High CVP chokes venous drainage → ↓ flow → ↓ filtration.

Low flow mimics “dry” physiology, but the right atrial pressure shows the truth.

High CVP + low urine output means:

• The kidney is congested

• Forward flow is poor

• Perfusion pressure is low

• It is a fluid overload / venous congestion problem, not hypovolemia

Eg (Venous congestion); 

• sepsis + positive fluids

• heart failure

• renal failure

• liver failur

• post-resuscitation state

• mechanical ventilation

Shock Problem & Best Tool

• Unclear preload: PLR, VTI

• Unclear fluid need: PPV/ SVV / NICOM

• LV function: Echo

• RV function: Echo + VExUS

• Flow failure: CO monitors (Echo, NICOM, PAC)

• Congestion: CVP + VExUS

• Tissue perfusion: Lactate, ScvO₂, CRT

• Renal perfusion: RRI, VExUS

Hemodynamic monitoring

1)  Identify Shock

• MAP <65

• CRT >3 sec

• Cold extremities

• Low UO

• Altered sensorium

• Lactate ↑

If any of these are abnormal → treat as true shock.

2) Immediate clues

• CVP/JVP

  • • • Low → likely dry (unless RV failure)

      • High → congestion / RV problem / tamponade

• Skin temp

  • • • Warm = distributive

      • Cold = low-flow state

3) Echo

• LV empty? (kissing walls → give fluids)

• LV weak? (poor squeeze → inotrope)

• RV enlarged? (bowing septum → NO fluids)

• IVC flat or full?

• Pericardial effusion? (tamponade → drain)

4) Is the patient fluid responsive?

• Use dynamic markers, not CVP:

• Passive Leg Raise (PLR) with VTI or NICOM

  • • ↑ SV ≥10% → give fluid

    • PPV/SVV >13% (on controlled ventilation)

• End-expiratory occlusion test

• Respiratory VTI variation >12–15%

• If not responsive → Stop fluids.

5)What is happening to the flow? (CO/SV)

• Echo VTI trend

• NICOM (PLR-friendly)

• FloTrac/Vigileo

• PiCCO (ARDS / septic shock)

• PAC/Swan-Ganz (severe RV failure, PH)

• Use these to titrate pressors + inotropes.

6) Tissue perfusion targets

• Lactate clearance

• ScvO₂ >70%

• CRT <3 sec

• Warm extremities

• Improving mental status

• If these stay poor → escalation is needed.

7) Check for congestion (avoid fluid overload)

• VExUS score (IVC + hepatic + portal Doppler)

• High CVP

  • • Renal vein congestion

    • Rising creatinine + high CVP → Stop fluids; start diuresis; reduce PEEP; improve RV output.

8) Lung-heart interaction

• High PEEP → worsens RV preload + output

• Look for:

  • • RV dilation

    • Septal flattening

    • Low TAPSE

If RV failing → avoid fluids; use vasopressor + inodilator (dobutamine).

9) Renal perfusion check

• RRI >0.75 → poor renal perfusion

• MAP – CVP = renal perfusion pressure

• If RPP is low → improve MAP or reduce CVP

• Combine with VExUS for congestion.

10) Final integration - Intervention

• Hypovolemic: Fluids (if PLR +ve), norepinephrine if needed

• Distributive (septic): Norepinephrine first, fluids only if responsive

• Cardiogenic: Avoid fluids; use inotropes + pressors

• Obstructive: Fix cause (tamponade, PE, tension)

• RV Failure: Stop fluids; improve RV; decrease PEEP

Standardised symbols (Each letter actually means something precise) for oxygen transport

C = Content

Always means “how much of something per unit blood volume.”

• CaO₂ = arterial oxygen content

• CvO₂ = venous oxygen content

• CcO₂ = capillary/alveolar end-capillary oxygen content

• CtO₂ = total mixed content

Subscript “a”, “v”, “c”, “t” (These tell you which blood compartment you are talking about)

• a = arterial

• v = venous (mixed venous unless specified SvO₂)

• c = capillary / pulmonary capillary

• t = total (mixed)

P = partial pressure (PaO₂, PvO₂)

S = saturation (SaO₂, SvO₂)

V̇ = flow/ventilation

Q̇ = perfusion/cardiac output

F = fraction (FiO₂)

D = diffusing capacity (DLCO)

Partial pressure = P (Gas pressure in plasma — determines diffusion.)

• PaO₂ Arterial partial pressure

• PvO₂ Venous partial pressure

• PAO₂ Alveolar partial pressure

Saturation = S % of Hb occupied by O₂ (0–100%)

The easiest bedside estimate of O₂ transport.

Acid, fever, hypercapnia shift curve → change S at same P.

• SaO₂ Arterial O₂ saturation

• SvO₂ Venous saturation (central/mixed)

• ScvO₂ Central venous saturation

Cardiac output = Q (Blood flow carrying oxygen)

Low Q̇ = low DO₂ even if lungs are perfect.

• Q̇ Cardiac output

• Qs/Qt Shunt fraction

• QT Total pulmonary blood flow

Ventilation = V (movement of air)

Determines PaCO₂ (via V̇A).

V/Q problems → hypoxemia.

• V̇A: Alveolar ventilation

• V̇E : Minute ventilation

• V̇CO₂: CO₂ production

• V̇O₂: Oxygen consumption

Diffusion capacity = D

How well gases cross the alveolar membrane. 

A surrogate for oxygen diffusion

• DLCO: Diffusing capacity for CO (surrogate for O₂ diffusion)

Letter V

In physiology:

V̇ = flow rate = volume / time

Examples:

V̇E = minute ventilation

V̇CO₂ = CO₂ production

V̇O₂ = oxygen consumption

VO₂ = volume of oxygen used per minute