Hemodynamic monitoring in emergency department from tintinalli and Rosen's emergency book

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Hemodynamic Monitoring in the Emergency Department

Source: Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Chapter 32 - "Hemodynamic Monitoring" (Hamade & Huang); with supplementary context from Rosen's Emergency Medicine

Introduction

Hemodynamic monitoring identifies cardiovascular insufficiency and facilitates optimal treatment of the critically ill. Advanced techniques help sort through various causes of hemodynamic instability and enable tailored interventions.

The key monitoring approaches applicable in the ED include:

Blood pressure monitoring
Central venous pressure (CVP) monitoring
Cardiac output (CO) monitoring
Blood oxygenation and lactate monitoring

In practice, using more than one approach and monitoring therapeutic responses gives the most reliable picture.

1. Arterial Blood Pressure

Blood pressure is the force exerted by circulating blood through vessels. Hypotension always reflects a failure of normal circulatory homeostatic mechanisms. Shock is a state of organ hypoperfusion that can occur even with a normal blood pressure (e.g., cardiogenic or hypovolemic shock with marked vasoconstriction).

Optimal MAP Targets

Clinical Context	Target
Septic shock (general)	MAP ≥ 65 mm Hg
Septic shock + chronic hypertension	MAP 75-85 mm Hg (reduces kidney injury)
Hemorrhagic shock (preoperative)	SBP 80-90 mm Hg (permissive hypotension)
Traumatic brain injury	SBP > 110 mm Hg
TBI age 50-69	SBP ≥ 100 mm Hg
Hemorrhagic shock + TBI	MAP > 80 mm Hg

MAP Formula:

MAP = Diastolic BP + [Pulse Pressure / 3]

MAP varies by only 1-2 mm Hg whether measured centrally or peripherally, making it a more reliable target than systolic BP in critically ill patients.

Noninvasive Blood Pressure Measurement

Palpation: Traditional teaching links palpable radial/femoral/carotid pulses to minimum SBP of 80/70/60 mm Hg respectively - but studies show these values overestimate actual SBP and are no longer in ATLS guidelines.

Sphygmomanometry: Auscultation using Korotkoff sounds. Important caveats:

Too small a cuff = falsely elevated readings
Too large a cuff = falsely low readings
Sphygmomanometric SBP tends to be slightly higher and diastolic slightly lower than direct arterial measurement

Oscillometry: Most automated monitors use this. The point of maximum cuff oscillation corresponds to MAP. Calculated MAP shows better correlation with invasive arterial monitoring than SBP, making it more reliable in critically ill patients.

Invasive Blood Pressure Measurement (Arterial Catheter)

The arterial catheter measures MAP and pulse pressure, estimates CO, and enables repeated blood sampling. Indications include:

Continuous BP monitoring in hemodynamically unstable patients
Frequent blood gas sampling needs
Requirement for beat-to-beat pressure monitoring

The radial artery is the most common site. The femoral and dorsalis pedis arteries are alternatives.

2. Central Venous Pressure (CVP)

CVP reflects right heart filling pressure and is used to estimate preload. Normal CVP is 2-8 mm Hg (or ~3-10 cm H₂O).

Important limitation: The relationship between CVP and preload depends heavily on cardiac compliance. The same volume (e.g., 80 mL) may produce very different CVP readings depending on diastolic compliance. Therefore, CVP alone is an unreliable static predictor of fluid responsiveness.

Dynamic use: Respiratory variation in CVP is more useful than an absolute value:

CVP variation with respiration suggests the heart is on the steep (preload-dependent) part of the cardiac function curve, and will likely respond to volume
Lack of respiratory variation suggests preload independence - the heart is volume-resuscitated

Noninvasive CVP Estimation

Jugular Venous Pulsation (JVP): The sternal angle is approximately 5 cm above the center of the right atrium regardless of patient position. With the patient at 45 degrees:

CVP (cm H₂O) = Vertical height of pulsation above sternal angle + 5 cm

A pulsation > 4.5 cm above the sternal angle at 45 degrees = CVP > 9.5 cm H₂O.

Elevated JVP in heart failure is independently associated with hospitalization and death.

Ultrasonography of the IVC:

IVC diameter < 2 cm with > 50% inspiratory collapsibility = CVP < 10 cm H₂O (low preload state)
Distended jugular vein (larger than adjacent carotid) on transverse US in semi-upright position = CVP > 10 cm H₂O
Nearly collapsed IVC on transverse view in supine position = very low CVP

3. Cardiac Output (CO) and Volume Responsiveness

Starling Curve and Preload Dependence

The Starling cardiac function curve illustrates that early increases in preload produce large increases in CO (preload-dependent zone), while further increases beyond optimal preload produce diminishing returns. The goal is to determine whether a patient will benefit from further fluid administration.

Dynamic Predictors of Fluid Responsiveness

Passive Leg Raising (PLR)

PLR acts as an "autotransfusion" test that temporarily increases venous return. Changes in CO during PLR persist for approximately 2-3 minutes. Dynamic increases in CO with PLR are as sensitive and specific for predicting volume responsiveness as pulse pressure variation (PPV), but can be used in spontaneously breathing patients.

Pulse Pressure Variation (PPV) - Mechanically Ventilated Patients

Positive-pressure ventilation induces predictable cyclic changes in vena caval diameter, pulmonary blood flow, and LV output.

PPV = (PP_max - PP_min) / PP_mean over one respiratory cycle

PPV > 13% predicts a > 15% increase in CO in response to a 500-mL crystalloid bolus
Continuing fluids until PPV decreases to < 10% may improve outcomes
Requirement: patient must be on controlled mechanical ventilation (not spontaneously triggering breaths)

IVC Ultrasonography (Spontaneously Breathing)

Small IVC (< 2 cm) with low minimal respiratory variation = hypovolemic state, potentially fluid responsive
Used alongside PLR for functional hemodynamic assessment

4. Blood Oxygenation and Lactate Monitoring

Blood pressure, CVP, and CO are macrohemodynamic parameters. Venous oxygen saturation and blood lactate are used to indirectly assess tissue oxygenation and perfusion adequacy.

Central Venous Oxygen Saturation (ScvO₂)

ScvO₂ is measured from the internal jugular or subclavian vein central catheter as a surrogate for mixed venous oxygen saturation (SvO₂ measured in the pulmonary artery).

Normal oxygen extraction ratio: 25-35%
Normal ScvO₂: approximately 70% (reflecting 70% return of arterial oxygen delivery)
ScvO₂ is typically 2-3% less than SvO₂ in healthy individuals, but 5-10% higher than SvO₂ in shock (due to redistribution of blood flow away from splanchnic circulation toward brain and heart)

Causes of Abnormal ScvO₂:

Low ScvO₂ (< 70%)	High ScvO₂ (> 70%)
Low DO₂: Hypoxia, anemia, hemorrhage, cardiac dysfunction, hypovolemia, tamponade	High DO₂: Hyperoxia, erythrocytosis, hyperdynamic state
High VO₂: Exercise, pain, hyperthermia, shivering, seizure	Low VO₂: Hypothermia, anesthesia/paralysis, AV shunting, mitochondrial dysfunction, terminal shock

Clinical use: The principal value of ScvO₂ is to detect occult inadequate oxygen delivery. A low ScvO₂ prompts troubleshooting of oxygen delivery (hemoglobin, SaO₂, CO) and/or oxygen consumption (metabolic demand).

Lactate

Lactate reflects tissue oxygen debt. Elevated lactate (> 2 mmol/L) suggests tissue hypoperfusion and is used as an endpoint of resuscitation. Serial lactate measurements (lactate clearance) guide treatment response better than any single value.

5. Summary Table: Hemodynamic Variables Obtainable in the ED

Variable	Method
Blood pressure (mmHg)	Sphygmomanometry, oscillometry, arterial line
MAP	Formula (DBP + PP/3) or direct arterial line
CVP	JVP estimation, IVC ultrasound, or CVC manometry
Volume responsiveness	PLR, PPV, IVC collapsibility index
Cardiac output	Thermodilution (PA catheter), echocardiography, pulse contour analysis
ScvO₂	Central venous catheter co-oximetry
Lactate	Arterial or venous blood gas

Rosen's Emergency Medicine - Key Supplementary Points

Rosen's emphasizes that in the ED, initial monitoring should include:

Pulse oximetry
Continuous ECG
Noninvasive BP monitoring

In the critical care / resuscitation bay, adding:

Intra-arterial BP monitoring
End-tidal CO₂ (ETCO₂) monitoring
CVP monitoring
ScvO₂ from the superior vena cava

Rosen's notes that ultrasound-assisted central access reduces average access time, number of attempts, and mechanical complications compared to landmark technique.

For patients with complex physiology (heart failure, renal failure), the Rapid Ultrasound for Shock and Hypotension (RUSH) examination or invasive hemodynamic monitoring should guide fluid therapy. - Rosen's Emergency Medicine

Key Takeaways:

No single hemodynamic parameter is sufficient; use multimodal monitoring
Dynamic measures (PPV, PLR, IVC collapsibility) outperform static measures (CVP, CVP alone) for predicting fluid responsiveness
MAP is a more reliable target than SBP in critically ill patients
ScvO₂ detects occult tissue oxygen debt even when macrohemodynamics appear stable
Permissive hypotension (SBP 80-90) applies specifically to pre-operative hemorrhagic shock, but TBI requires higher targets

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