5 Hemodynamic Measurements and Interpretation

How pressure, flow, and resistance relate

Hemodynamics describes the interaction of blood pressure, blood flow, and vascular resistance in perfusing organs. A single measurement rarely explains a patient's condition: interpret values together, check whether they are changing, and compare them with the examination and the patient's baseline.

Core relationships

Cardiac output (CO) is the volume of blood pumped per minute. It is calculated as:

A typical adult resting cardiac output is about $4\text{–}8\ \mathrm{L/min}$, but it varies with body size, activity, and metabolic demand. Bedside methods estimate cardiac output and may disagree. Stroke volume (SV) can be calculated as cardiac output divided by heart rate, so a normal cardiac output can mask a low stroke volume when heart rate is high.

Cardiac index (CI) adjusts cardiac output for body surface area:

This adjustment is useful when comparing people of different sizes.

Mean arterial pressure (MAP) approximates average arterial pressure over a cardiac cycle. At ordinary heart rates, it can be estimated from systolic and diastolic blood pressure:

For a blood pressure of $120/75\ \mathrm{mmHg}$, the estimated MAP is $90\ \mathrm{mmHg}$. This is an approximation, not a stand-alone assessment of perfusion.

MAP reflects both flow and resistance. A useful approximation is:

Unit conversions are required for clinical calculations. Because resistance affects pressure, a reasonable MAP can coexist with low cardiac output when vascular resistance is high.

Cardiac loading conditions

Preload is myocardial stretch at end-diastole. Ventricular filling volume is conceptually closer to preload than filling pressure; right atrial pressure, also called central venous pressure (CVP), and pulmonary artery wedge pressure (PAWP) are imperfect pressure-based surrogates.

Increasing preload can raise stroke volume when the ventricle is on the ascending part of its Frank–Starling relationship. It may have little effect or cause harm when the heart is already volume-replete or failing.

Afterload is the load opposing ventricular ejection. Systemic vascular resistance (SVR) approximates left-ventricular arterial load, while pulmonary vascular resistance (PVR) approximates right-ventricular vascular load. Neither is a complete measure of myocardial afterload. Increasing afterload can reduce stroke volume, especially when contractility is impaired.

Common measurements and reference patterns

The following are approximate adult reference patterns, not universal treatment targets. Age, body size, ventilation, position, disease, and measurement technique affect interpretation. Pressure values are in $\mathrm{mmHg}$ unless another unit is given.

• Heart rate (HR): $60\text{–}100\ \mathrm{beats/min}$. Tachycardia may compensate for low stroke volume or increased demand, but it can also shorten filling time. Rhythm matters.

• Arterial blood pressure and MAP: Interpret against the patient's baseline and clinical context. Hypotension can signal inadequate perfusion, but normal blood pressure does not rule out poor flow or early deterioration.

• Cardiac output (CO): About $4\text{–}8\ \mathrm{L/min}$. It represents total flow and should be interpreted in relation to body size and metabolic needs.

• Stroke volume (SV): About $60\text{–}100\ \mathrm{mL/beat}$. It can be calculated as $\mathrm{CO}/\mathrm{HR}$.

• Right atrial pressure or CVP: About $1\text{–}6\ \mathrm{mmHg}$. It reflects right-sided pressure, not circulating blood volume, and is influenced by right-heart function, venous tone, intrathoracic pressure, and positive end-expiratory pressure (PEEP).

• Right-ventricular pressure: Systolic $15\text{–}30\ \mathrm{mmHg}$ and diastolic $1\text{–}6\ \mathrm{mmHg}$. Elevated values may reflect increased pulmonary load or impaired right-heart function; interpret the waveform and clinical picture.

• Pulmonary artery pressure: Systolic $15\text{–}30\ \mathrm{mmHg}$, diastolic $6\text{–}12\ \mathrm{mmHg}$, and mean $10\text{–}20\ \mathrm{mmHg}$. An elevated value alone does not identify the cause.

• PAWP: About $6\text{–}12\ \mathrm{mmHg}$. It estimates left atrial pressure under appropriate conditions; it is not a direct measure of left-ventricular filling volume and may not equal left-ventricular end-diastolic pressure.

• SVR: Roughly $800\text{–}1200\ \mathrm{dyn\cdot s\cdot cm^{-5}}$. It is derived from pressure and cardiac output, so errors in either affect the result.

• PVR: Usually less than $250\ \mathrm{dyn\cdot s\cdot cm^{-5}}$. Its reliability depends on accurate measurements of all inputs.

• Mixed venous oxygen saturation (SvO₂): About $65\text{–}80\%$. It reflects the balance of oxygen delivery and consumption; a low or falling value is concerning but nonspecific. ScvO₂ is not interchangeable with SvO₂.

The derived resistance calculations are:

CVP and PAWP are pressure measurements, not stand-alone tests of fluid responsiveness.

Monitoring methods and limitations

Clinical assessment and basic monitoring provide essential context. Repeated vital signs, ECG, oxygen saturation, skin temperature and color, capillary refill, mental status, and urine output should be considered together. ECG shows rate and rhythm; it does not establish whether the resulting contractions produce adequate blood flow.

• Noninvasive cuff blood pressure: Convenient and intermittent. Motion, poor perfusion, cuff size or placement, and rapidly changing status can reduce reliability or delay recognition of a trend.

• Arterial catheter: Provides continuous pressure waveforms and enables arterial blood sampling. Accuracy depends on correct leveling, zeroing, and waveform quality; a misplaced transducer or poorly damped system can distort readings.

• Central venous catheter: Measures CVP when correctly positioned and referenced. CVP changes with breathing and positive-pressure ventilation and does not reliably indicate whether a patient needs fluid.

• Bedside echocardiography: Assesses cardiac structure, function, and flow patterns without a catheter. It depends on the operator and available views, and is usually a snapshot rather than continuous monitoring.

• Pulmonary artery catheter (PAC): Can measure right-sided and pulmonary artery pressures, PAWP, SvO₂, and thermodilution cardiac output. It is invasive; readings depend on catheter position, transducer setup, respiratory phase, and correct waveform identification. PAWP may not reflect left-ventricular end-diastolic pressure when the relevant assumptions are not met. Thermodilution has limitations, including in some cases of valve regurgitation and intracardiac shunts.

• Dynamic measures of fluid responsiveness: Changes in stroke volume or pulse pressure during a controlled maneuver can be more informative than one static filling pressure. Their usefulness depends on conditions such as rhythm, ventilation, and measurement method; they are not valid in every patient.

For invasive pressure readings, zero and level the transducer at the heart reference level, then assess the waveform before interpreting it. When comparing serial values, keep positioning and measurement conditions as consistent as possible. Pulmonary artery catheter readings and thermodilution methods have specific sources of error; when the method is consistent, a trend may be more useful than a single number.

Recognizing deterioration

Respond to a worsening pattern rather than waiting for one threshold. Concerning findings can include falling blood pressure or MAP, rising or unusually low heart rate, a new arrhythmia, declining oxygen saturation, altered mentation, cool or mottled skin, delayed capillary refill, increasing lactate, or falling urine output.

Hypotension, tachycardia, and lactate elevation are not individually diagnostic. Consider trends and the whole clinical picture. Urine output below $0.5\ \mathrm{mL\cdot kg^{-1}\cdot hour^{-1}}$ over time is a warning sign that warrants assessment, not a diagnosis by itself. Follow local escalation procedures promptly when deterioration is suspected.

Applying the measurements

These calculations illustrate how to use the relationships and measurements; they do not determine treatment.

1. Calculate flow: If heart rate is $100\ \mathrm{beats/min}$ and stroke volume is $60\ \mathrm{mL/beat}$, then:

   $$\mathrm{CO}=100\times60=6000\ \mathrm{mL/min}=6\ \mathrm{L/min}$$

2. Estimate MAP: For a blood pressure of $90/60\ \mathrm{mmHg}$:

   $$60+\frac{1}{3}(90-60)=70\ \mathrm{mmHg}$$

   This estimate alone does not establish adequate perfusion.

3. Interpret pressure versus volume: An elevated CVP in a ventilated patient receiving PEEP does not prove excess circulating volume. PEEP and intrathoracic pressure can raise measured CVP, and right-heart function and other factors also affect it. Interpret the measurement alongside the examination and other findings.

4. Assess possible low flow: A blood pressure of $110/70\ \mathrm{mmHg}$ does not by itself reassure when heart rate is $125\ \mathrm{beats/min}$ and the patient is newly confused with cool extremities. These signs may indicate deterioration despite a seemingly acceptable pressure; reassess promptly and escalate according to local practice.

5. Consider afterload: If SVR rises while contractility and preload remain unchanged, the ventricle faces greater resistance to ejection, so stroke volume may fall, particularly if contractile function is impaired.

6. Calculate SVR: For cardiac output of $3\ \mathrm{L/min}$, MAP of $75\ \mathrm{mmHg}$, and right atrial pressure of $5\ \mathrm{mmHg}$:

   $$80\times\frac{75-5}{3}=1867\ \mathrm{dyn\cdot s\cdot cm^{-5}}$$

   This is above the approximate reference range given earlier. Check the calculated value against measurement quality and the clinical context.

Putting the findings together

Hemodynamic interpretation links pressure, flow, and resistance: cardiac output equals heart rate multiplied by stroke volume, while MAP depends on both cardiac output and vascular resistance. Preload and afterload describe cardiac loading conditions, but common bedside pressures are imperfect surrogates. Select monitoring to answer a clinical question, verify measurement quality, and interpret serial values alongside signs of organ perfusion. A concerning trend or new sign of deterioration merits prompt reassessment and escalation.