01 / CLINICAL CASE
One patient, changing physiology
STAGE 1
At presentation
A 50-year-old man presents after a high-speed motor vehicle collision with pelvic fractures, splenic bleeding, and rib fractures. He is cold and mottled, with fluctuating consciousness.
- Heart rate
- 128 beats/min
- Blood pressure
- 78/45 mmHg
- Respiratory rate
- 26/min
- Oxygenation
- SpO₂ 95% on a non-rebreather
- Hemoglobin
- 8.2 g/dL
- Lactate
- 5.8 mmol/L
- Blood gas
- pH 7.21 · PaCO₂ 29 · PaO₂ 85 mmHg
- ScvO₂
- 55%
Pulmonary artery catheter measurements
- CVP
- 3 mmHg
- PA pressure
- 18/6 (mean 10) mmHg
- PAWP
- 5 mmHg
- Cardiac output / index
- 3.2 L/min / 1.6 L/min/m²
- SVR (estimated MAP)
- 1,325 dyn·s·cm⁻⁵
- SvO₂
- 48%
What would a pulmonary artery catheter change about your initial priorities?
Discussion
Low filling pressures, low flow, and reduced mixed venous oxygen saturation support hemorrhagic shock in the setting of active bleeding. The clinical history already identifies the immediate problem.
STAGE 2
After resuscitation and hemorrhage control
After resuscitation, splenic artery embolization, and a pelvic binder, he is warm and alert. Oxygen requirement falls to 2 L/min by nasal cannula.
- Heart rate
- 95 beats/min
- Blood pressure
- 102/62 mmHg
- Hemoglobin
- 9.1 g/dL
- Lactate
- 2.1 mmol/L
- ScvO₂
- 71%
Pulmonary artery catheter measurements
- CVP
- 8 mmHg
- PA pressure
- 26/12 (mean 16) mmHg
- PAWP
- 10 mmHg
- Cardiac output / index
- 5.4 L/min / 2.7 L/min/m²
- SVR (estimated MAP)
- 998 dyn·s·cm⁻⁵
- SvO₂
- 68%
Which bedside findings tell you that perfusion has improved?
Discussion
Perfusion, lactate, and cardiac output improve together. Reassessment of the patient remains central to interpreting the numbers.
✦ Physiology pit stop
Compare the filling pressures; connect the forward flow.
Compare both sides of the circulation. Filling pressures need not match, even though sustained forward flow through the two circuits must balance in a steady state without a shunt.
A quick concept to take to the bedside.STAGE 3
New deterioration on ICU day 5
After three days without vasopressors, he develops fever, oliguria, and increasing oxygen requirements. A central line and urinary catheter have remained in place since admission. His extremities are warm with bounding pulses.
- Temperature
- 39.2 °C
- Heart rate
- 118 beats/min
- Blood pressure
- 86/50 mmHg on norepinephrine 5 µg/min
- Oxygenation
- SpO₂ 93% on 4 L/min
- WBC
- 19.6 × 10⁹/L
- Lactate
- 4.0 mmol/L
- ScvO₂
- 78%
- Initial source evaluation
- Clear chest radiograph, bland urinalysis, clean line site
Pulmonary artery catheter measurements
- CVP
- 12 mmHg
- PA pressure
- 30/16 (mean 20) mmHg
- PAWP
- 14 mmHg
- Cardiac output / index
- 7.0 L/min / 3.5 L/min/m²
- SVR (estimated MAP)
- 571 dyn·s·cm⁻⁵
- SvO₂
- 78%
Does the catheter resolve an uncertainty that the examination and initial investigations leave unanswered?
Discussion
High flow with hypotension and fever supports a distributive physiology. A high venous oxygen saturation does not establish adequate tissue perfusion. The source of infection still requires investigation.
STAGE 4
Persistent bacteremia and a new murmur
Blood cultures grow MSSA in two sets. The central line is removed. Fever persists, vasopressor and oxygen requirements rise, and a new early diastolic murmur appears. He becomes cool and mottled, with bibasilar crackles and slowing cognition.
- Blood pressure
- 98/45 mmHg
- Support
- Norepinephrine 15 µg/min and vasopressin 0.03 units/min
- Oxygenation
- SpO₂ 94% on 6 L/min
- Lactate
- 5.2 mmol/L
- Hemoglobin
- 8.7 g/dL
- Bedside echo
- LVEF about 40%, mobile aortic valve elements, severe aortic regurgitation, without marked LV dilation
Pulmonary artery catheter measurements
- CVP
- 20 mmHg
- PA pressure
- 35/26 (mean 29) mmHg
- PAWP
- 25 mmHg
- Cardiac output / index
- 2.0 L/min / 1.0 L/min/m²
- SVR (estimated MAP)
- 1,707 dyn·s·cm⁻⁵
- SvO₂
- 58%
How does the new valve finding change your interpretation of the shock state?
Discussion
The pattern has changed to low flow with elevated filling pressures. Severe aortic regurgitation and MSSA bacteremia raise concern for infective endocarditis with a cardiogenic component superimposed on sepsis. The high calculated SVR reflects the current low-flow, vasopressor-supported state; it does not exclude concurrent infection. Urgent endocarditis and surgical assessment are needed for acute severe AR.
02 / PHYSIOLOGY FIRST
Assessment begins at the bedside
Assess perfusion and congestion together, then reconcile the examination with laboratory findings and echocardiography.
- Perfusion
- Mental status, skin temperature and mottling, pulse volume, urine output, and lactate trend.
- Congestion
- Jugular venous pressure, pulmonary crackles, work of breathing, and oxygen requirement.
- Cardiac clues
- Murmurs, extra heart sounds, pulse contour, heaves, and thrills.
- Trajectory
- Changes in blood pressure, heart rate, organ function, and the amount of support required.
Perfusion and congestion
Use left and right arrow keys to change congestion, up and down to change perfusion. Shift moves ten steps. Home selects warm and dry; End selects cold and wet. Current cardiac index 3.0 liters per minute per square meter; wedge 11 millimeters of mercury.
Clinical profiles adapted from Lilly. These descriptors summarize an examination rather than establish an etiology.
✦ High-yield pearl
One number rarely tells the whole physiological story.
Read pressure alongside flow, perfusion and the clinical story. Two patients can share a pressure value and have very different problems.
A quick concept to take to the bedside.03 / INVASIVE ASSESSMENT
Reading pressures in context
Measured and derived quantities
- Pressure and saturation
- CVP, pulmonary artery pressure, PAWP, and mixed venous oxygen saturation (SvO₂).
- Flow
- Cardiac output by thermodilution or by the Fick method. The method and its assumptions matter.
- Derived variables
- Cardiac index = CO / body surface area. Stroke volume = CO × 1,000 / heart rate. SVR and PVR relate pressure gradients to flow.
The right atrial waveform
- a wave
- Atrial contraction.
- c wave
- Tricuspid valve bulging toward the right atrium during early ventricular systole.
- x / x′ descents
- Atrial relaxation (x), followed by systolic downward displacement of the tricuspid annulus (x′); terminology varies across sources.
- v wave
- Right atrial filling while the tricuspid valve is closed.
- y descent
- Right atrial emptying after the tricuspid valve opens.
Right atrium tracing
Right ventricle tracing
Pulmonary artery tracing
Pulmonary artery wedge tracing
Read the waveform with the ECG and the clinical context. A prominent wedge v wave can accompany mitral regurgitation, but it is not diagnostic on its own.
PADP, PAWP and LVEDP
Pulmonary hypertension: pressure, wedge, and resistance
Resting pulmonary hypertension requires mean PA pressure >20 mmHg. Precapillary physiology also requires PAWP ≤15 mmHg and PVR >2 Wood units. With PAWP >15 mmHg, PVR distinguishes isolated postcapillary physiology (≤2 WU) from combined post- and precapillary physiology (>2 WU).
2022 ESC/ERS pulmonary hypertension guidelines. Hemodynamics alone do not establish the clinical PH group.
04 / CARDIOGENIC SHOCK
Low flow and organ hypoperfusion
Cardiogenic shock is circulatory failure due to cardiac dysfunction with inadequate tissue perfusion. Look for altered mentation, cool extremities, oliguria, and rising lactate, alongside evidence of impaired cardiac performance.
Five stages. One evolving patient.
At risk
Risk of shock, with perfusion and blood pressure maintained.
No current signs of cardiogenic shock.Beginning
Hypotension or tachycardia, with tissue perfusion still maintained.
Hemodynamic instability without hypoperfusion.Classic
Hypoperfusion requiring drug or device support beyond volume resuscitation.
Hypotension is common, but is not required.Deteriorating
Initial support fails to restore perfusion; treatment must escalate.
Persistent or worsening hypoperfusion despite initial therapy.Extremis
Circulatory collapse is imminent or already occurring.
Profound instability despite intensive resuscitation.
Reassess severity over time. Increasing support needs and worsening perfusion are central to recognizing deterioration.
05 / WORKED EXAMPLES
Pressure, flow, and resistance
Keep units visible. Use oxygen saturations as fractions in the Fick equation and mixed venous blood for SvO₂. ScvO₂ is a different measurement.
Fick cardiac output
- Oxygen consumption
- 125 mL/min/m² × 2 m² = 250 mL/min
- Hemoglobin
- 150 g/L (15 g/dL)
- Arterial / mixed venous saturation
- 0.99 / 0.60
- Calculation
- 250 / [1.36 × 150 × (0.99 − 0.60)]
- Cardiac output
- 3.14 L/min
Systemic vascular resistance
For BP 130/70 mmHg, estimated MAP is 90 mmHg. With CVP 8 mmHg and CO 3.14 L/min:
80 × (90 − 8) / 3.14 ≈ 2,089 dyn·s·cm⁻⁵
Pulmonary vascular resistance
For mean PA pressure 17 mmHg, PAWP 12 mmHg, and CO 3.14 L/min:
(17 − 12) / 3.14 ≈ 1.59 Wood units
Multiply by 80: approximately 127 dyn·s·cm⁻⁵
✦ Unit check
Same resistance, different units.
Multiply Wood units by 80 to obtain dyn·s·cm⁻⁵. The physiology stays the same; only the units change.
A quick concept to take to the bedside.FROM THE REFERENCE LIBRARY
Pressure is only part of the story
Use the contour, its timing, and the measurement method to decide what a pressure or output value actually represents.
Wedge, LVEDP, and the v wave
Mean wedge reflects the left atrial pressure burden across the cardiac cycle. LVEDP is a ventricular pressure at end-diastole. A large wedge v wave can raise the mean above LVEDP; it does not, by itself, establish severe MR. A stiff left atrium can produce a large v wave, while a compliant, enlarged atrium can accommodate severe MR with a less prominent wave.
Stouffer, Cardiovascular Hemodynamics for the Clinician (2008), chapter 5, p. 71.
Why a wedge–LV comparison can suggest a false mitral gradient
The wedge waveform reaches the catheter after the corresponding left atrial event. Comparing it with LV pressure without accounting for this delay can create an apparent diastolic gradient. Assess properly timed diastolic pressures; mean wedge minus LVEDP is not a measured mean transmitral gradient.
Ragosta, Textbook of Clinical Hemodynamics, 2nd ed. (2018), p. 36, figures 2.28–2.29.
Before accepting a measurement
| Check | Why it matters |
|---|---|
| Level, zero, and timing | A transducer below the reference level reads too high; one above it reads too low. Record respiratory timing and ventilatory support. |
| Scale and ECG | A scale suited to LV systolic pressure can hide atrial waves. Identify pressure events against the ECG rather than by shape alone. |
| Ringing or catheter motion | Spurious systolic spikes and low troughs may exaggerate pulse pressure or suggest a false gradient. |
| Output method | Repeat technically consistent thermodilution measurements. In TR, low flow, or an irregular rhythm, scrutinize disagreement rather than applying a universal correction factor. |
Stouffer (2008), p. 26; Ragosta (2018), pp. 39 and 59–60.
Lower filling pressure can coexist with higher flow
Steimle and colleagues reassessed 25 transplant-free survivors with advanced heart failure after tailored diuretic and vasodilator therapy. Their serial measurements illustrate why a lower wedge need not mean a lower stroke volume.
| Measurement | Baseline | Early treatment | Follow-up |
|---|---|---|---|
| Wedge, mmHg | 24 ± 9 | 15 ± 5 | 12 ± 6 |
| Stroke volume, mL | 42 ± 10 | 56 ± 13 | 79 ± 20 |
| SVR, dyn·s·cm⁻⁵ | 1,651 ± 369 | 1,207 ± 281 | 1,003 ± 193 |
Early reassessment: 24–72 hours; later reassessment: 8 ± 6 months. Steimle et al. Circulation. 1997;96:1165–1172.
Discuss: has decongestion improved this patient?
Compare symptoms, perfusion, forward flow, filling pressures, and renal function over time. Falling wedge with improving flow supports a favorable response; falling wedge with worsening perfusion calls for reassessment. Neither a pressure target nor a single output measurement is sufficient.