8.2 Invasive Hemodynamics: Arterial Lines, CVP & Pulmonary Artery Catheters

8.2 Invasive Hemodynamics: Arterial Lines, CVP & Pulmonary Artery Catheters

Invasive hemodynamic monitoring provides beat-to-beat cardiovascular assessment during major surgical interventions, shock states, and complex cardiac procedures. Mastery of waveform analysis, physical damping principles, and intracardiac pressure dynamics allows the CRNA to optimize preload, afterload, inotropy, and tissue perfusion while avoiding catastrophic interpretation errors.

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1. Arterial Catheterization: Vascular Sites & Allen Test

Continuous direct arterial pressure monitoring is indicated for patients with severe hemodynamic instability, planned induced hypotension, severe cardiopulmonary disease, major vascular/cardiac surgery, or frequent arterial blood gas requirements.

+-------------------------------------------------------------------------+
|                        ARTERIAL CANNULATION SITES                       |
+------------------+------------------------------------------------------+
| Arterial Site    | Clinical Characteristics & Anesthetic Considerations |
+------------------+------------------------------------------------------+
| **Radial**       | • Most common site; superficial and easily accessible|
|                  | • Dual palmar arch collateral supply via ulnar artery|
| **Ulnar**        | • Principal blood supplier to the deep palmar arch   |
|                  | • Cannulation avoided if ipsilateral radial failed   |
| **Brachial**     | • End artery with no functional collateral network   |
|                  | • Risk of median nerve compression & forearm ischemia|
| **Femoral**      | • Large bore; reliable during profound shock/arrest  |
|                  | • Risks: Retroperitoneal hemorrhage, pseudoaneurysm  |
| **Axillary**     | • Left axillary preferred (reduces embolic stroke)   |
|                  | • Proximity to neurovascular bundle (brachial plexus)|
| **Dorsalis       | • Distal peripheral site; exhibits pronounced pulse  |
|   Pedis / PT**   |   pressure amplification (highest SBP, lowest DBP)   |
+------------------+------------------------------------------------------+

The Modified Allen Test

• Purpose: Assesses the patency and adequacy of collateral arterial blood flow to the hand via the ulnar artery and palmar arch prior to radial artery cannulation.
• Procedure: The clinician simultaneously occludes both the radial and ulnar arteries while the patient clenches their fist to exsanguinate the hand. With the hand open (avoiding hyperextension), the clinician releases pressure on the ulnar artery only while maintaining firm compression on the radial artery.
• Interpretation:
  • Normal / Adequate Collateral Flow: Hand reperfuses (turns pink) within $<5 - 10 \text{ seconds}$.
  • Equivocal / Borderline: Reperfusion takes $10 - 15 \text{ seconds}$.
  • Abnormal / Compromised Collateral Flow: Reperfusion requires $>15 \text{ seconds}$ (cannulation of that radial artery is contraindicated due to risk of digital ischemic necrosis).

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2. Arterial Waveform Morphology & Peripheral Pulse Pressure Amplification

                    [ARTERIAL PRESSURE WAVEFORM MORPHOLOGY]

      Pressure (mmHg)
        140 |
            |             Peak Systolic Pressure (SBP)
        120 |                 /\
            |                /  \
        100 |    Systolic   /    \   Dicrotic Notch (Aortic Valve Closure)
            |    Upstroke  /      \   /
         80 |    (Anacrotic)       \/\_  Diastolic Runoff
            |                      |   \_
         60 |                      |     \_ End-Diastolic Pressure (DBP)
            +----------------------+-------+-------------------> Time
                                Mechanical   Mechanical
                                 Systole      Diastole

Waveform Components

1. Anacrotic Limb (Systolic Upstroke): Steep initial upstroke representing ventricular ejection velocity and myocardial contractility ($dP/dt$).
2. Systolic Peak (SBP): Peak pressure generated during left ventricular ejection.
3. Dicrotic Limb & Dicrotic Notch (Incisura): The downward deflection interrupted by a notch created by closure of the aortic valve, marking the precise transition from mechanical systole to mechanical diastole.
4. Diastolic Runoff: Decline in arterial pressure governed by peripheral vascular resistance (SVR) and arterial compliance.
5. End-Diastolic Pressure (DBP): Trough pressure prior to the next ventricular contraction.

Peripheral Pulse Pressure Amplification

As the arterial pressure pulse wave travels distally from the central ascending aorta toward peripheral muscular arteries (e.g., radial, femoral, dorsalis pedis), it encounters decreasing arterial compliance (stiffer vessel walls) and reflective pressure waves bouncing back from arteriolar branch points.

+-------------------------------------------------------------------------+
|               CENTRAL AORTIC vs PERIPHERAL RADIAL WAVEFORM              |
+------------------------------------+------------------------------------+
| Central Aortic Pressure Waveform   | Peripheral Radial Pressure Waveform|
+------------------------------------+------------------------------------+
| • Lower Systolic Pressure (SBP)    | • Higher Systolic Pressure (SBP)   |
| • Higher Diastolic Pressure (DBP)  | • Lower Diastolic Pressure (DBP)   |
| • Narrower Pulse Pressure (PP)     | • Wider Pulse Pressure (PP)        |
| • Sharp, early Dicrotic Notch      | • Delayed, slurred Dicrotic Notch  |
| • MAP is CONSTANT (or drops ~1-2)  | • MAP is CONSTANT (mathematical)   |
+------------------------------------+------------------------------------+

NCE Clinical Principle — MAP Consistency: Although peripheral SBP is $10 - 20 \text{ mmHg}$ higher and peripheral DBP is $5 - 10 \text{ mmHg}$ lower than central aortic readings due to reflection wave summation, Mean Arterial Pressure (MAP) remains essentially unchanged across the arterial tree (with only a minuscule $1 - 2 \text{ mmHg}$ viscous drop). Thus, MAP is the true physiologic perfusion pressure.

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3. Dynamic Transducer Response: Natural Frequency & Damping

An invasive pressure monitoring system consists of an intravascular catheter, fluid-filled non-compliant pressure tubing, continuous flush device ($3 \text{ mL/hr}$ heparinized or plain saline at $300 \text{ mmHg}$ bag pressure), and an electromechanical strain-gauge transducer.

+-------------------------------------------------------------------------+
|                     UNDERDAMPED vs OVERDAMPED ARTIFACTS                 |
+-------------------+----------------------------+------------------------+
| Parameter         | Underdamped (Resonant/Ring)| Overdamped (Blunted)   |
+-------------------+----------------------------+------------------------+
| **Systolic (SBP)**| **Falsely ELEVATED**       | **Falsely DECREASED**  |
| **Diastolic(DBP)**| **Falsely DECREASED**      | **Falsely ELEVATED**   |
| **Pulse Pressure**| **Falsely WIDENED**        | **Falsely NARROWED**   |
| **Mean (MAP)**    | **ACCURATE / PRESERVED**   | **ACCURATE / PRESERVED**|
| **Physical Cause**| • Long tubing, stopcocks,  | • Air bubbles in line  |
|                   |   stiff non-compliant line | • Clots / fibrin sheath|
|                   | • Low natural frequency    | • Compliant soft tubing|
| **Flush Test**    | • >3 oscillations before   | • <1 oscillation / no  |
| **Waveform**      |   returning to baseline    |   ringing (slurred)    |
+-------------------+----------------------------+------------------------+

Physical Principles

• Natural Frequency ($f_n$): The frequency at which the transducer system freely oscillates when perturbed. To prevent distortion, the system's natural frequency must be at least 5 to 10 times higher than the fundamental cardiac frequency (ideally $>25 - 30 \text{ Hz}$).
• Damping Coefficient ($\zeta$): The measure of friction resisting fluid oscillation in the tubing (optimal damping coefficient is $0.64 - 0.70$).
• Square-Wave Flush Test: Activating the high-pressure flush valve generates a square wave. The number of baseline oscillations ("rings") following valve release determines damping status:
  • Optimally Damped: 1 to 2 oscillations before returning to baseline.
  • Underdamped: Multiple rapid, sharp oscillations ($>3$ rings) with overshooting systolic spikes.
  • Overdamped: Sluggish baseline return with zero oscillations and complete loss of the dicrotic notch.

Transducer Leveling & Hydrostatic Artifacts

• Reference Landmark: Transducers are leveled to the phlebostatic axis (4th intercostal space at the mid-axillary line, corresponding to the right atrium).
• Head-Up / Sitting Position (Craniotomy): Transducer must be zeroed and leveled at the External Auditory Meatus (Circle of Willis) to accurately assess Cerebral Perfusion Pressure ($CPP = MAP_{brain} - ICP$).
• Hydrostatic Conversion Factor:
  • $1.0 \text{ cm H}_2\text{O} = 0.74 \text{ mmHg}$
  • $1.0 \text{ inch} = 2.54 \text{ cm} \approx 1.86 - 2.0 \text{ mmHg}$
  • Transducer placed BELOW the patient: Falsely ELEVATES displayed blood pressure.
  • Transducer placed ABOVE the patient: Falsely LOWERS displayed blood pressure.

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4. Central Venous Pressure (CVP): Morphology & Kinetics

Central Venous Pressure measures hydrostatic filling pressure in the right atrium and vena cava, clinically approximating right ventricular preload (normal CVP: $2 - 6 \text{ mmHg}$ or $3 - 8 \text{ cmH}_2\text{O}$).

                     [CENTRAL VENOUS PRESSURE WAVEFORM]

         Pressure (mmHg)
           10 |
              |        a
            8 |       /\        v
              |      /  \  c   /\
            6 |     /    \/\  /  \
              |    /      x \/    \ y
            4 +---+----------+-----+-------> Time (ECG Correlation)
                 P-Wave    QRS   T-Wave

Normal CVP Waveform Components & Cardiac Timing

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5. Pathologic CVP Waveforms & NCE Board Recognition

+-------------------------------------------------------------------------+
|                        PATHOLOGIC CVP WAVEFORM PATTERNS                 |
+---------------------+---------------------------------------------------+
| Waveform Pathology  | Clinical Etiology & Diagnostic Features           |
+---------------------+---------------------------------------------------+
| **Cannon a waves**  | • Atrium contracts against a CLOSED tricuspid     |
|                     | • Third-Degree (Complete) AV Block, Junctional    |
|                     |   rhythm, Ventricular Pacing, PVCs, severe TS     |
| **Absent a waves**  | • Loss of coordinated atrial mechanical systole   |
|                     | • Atrial Fibrillation / Sinoatrial Arrest         |
| **Giant v waves**   | • Retrograde systolic jet from RV into RA         |
| **(Fusion Wave)**   | • Severe Tricuspid Regurgitation, noncompliant RA |
| **Kussmaul's Sign** | • Paradoxical RISE in CVP during spontaneous      |
|                     |   inspiration; Constrictive Pericarditis / RV MI  |
| **Tamponade Wave**  | • Prominent x descent, blunted/absent y descent   |
+---------------------+---------------------------------------------------+

NCE Board Distinction — Tamponade vs. Constrictive Pericarditis:

• Cardiac Tamponade: Elevated CVP with prominent $x$ descent and attenuated/absent $y$ descent (high intrapericardial pressure prevents early passive diastolic filling when tricuspid opens).
• Constrictive Pericarditis: Elevated CVP with sharp $x$ descent and steep, deep $y$ descent (creating an "M" or "W" waveform pattern and positive Kussmaul's sign).

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6. Pulmonary Artery Catheterization: Waveforms & Hemodynamics

A flow-directed Pulmonary Artery Catheter (PAC / Swan-Ganz) is advanced through the right internal jugular vein into the pulmonary circulation to measure intracardiac pressures, calculate vascular resistances, and determine cardiac output.

+---------------------------------------------------------------------------------------+
|                      PULMONARY ARTERY CATHETER INSERTION PROGRESSION                   |
+--------------------+---------------------+--------------------+-----------------------+
| Chamber / Vessel   | Distance from Rt IJ | Normal Pressure    | Waveform Features     |
+--------------------+---------------------+--------------------+-----------------------+
| **Right Atrium**   | $20 - 25 \text{ cm}$| $2 - 6 \text{ mmHg}$| Low-pressure a, c, v  |
| **Right Ventricle**| $30 - 35 \text{ cm}$| $25 / 0 - 5 \text{ mmHg}$| Tall systolic spike,  |
|                    |                     |                    | diastolic near zero   |
| **Pulmonary Artery**| $40 - 45 \text{ cm}$| $25 / 10 \text{ mmHg}$| Dicrotic notch present|
|                    |                     |                    | diastolic rises to 10 |
| **PAOP (Wedge)**   | $45 - 55 \text{ cm}$| $6 - 12 \text{ mmHg}$| Low-pressure LA wave  |
+--------------------+---------------------+--------------------+-----------------------+

   RA (2-6)        RV (25/0-5)         PA (25/10)        PAOP (6-12)
    /\  /\          /\     /\          /\     /\          /\  /\
   /  \/  \        /  \   /  \        /  \/\_/  \/\_     /  \/  \
  +--------+      +----+ +----+      +------------+     +--------+
                   (Diastolic ~0)     (Diastolic ~10
                                       w/ Dicrotic Notch)

West Zone 3 Catheter Positioning Requirement

For the pulmonary artery occlusion pressure (PAOP) to accurately reflect left atrial pressure (LAP) and left ventricular end-diastolic pressure (LVEDP), the PAC tip must be positioned in West Zone 3 of the lung ($P_a > P_v > P_A$).

• In West Zone 3, continuous, uninterrupted columns of blood connect the catheter tip directly to the left atrium through patent pulmonary veins.
• If the catheter is positioned in Zone 1 or Zone 2 ($P_A > P_v$), inflating the balloon causes alveolar pressure ($P_A$) to compress capillaries, causing the transducer to measure alveolar airway pressure rather than left heart filling pressure.

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7. Thermodilution Cardiac Output & Mixed Venous Saturation ($SvO_2$)

The Stewart-Hamilton Equation

Cardiac output is measured via the thermodilution technique by injecting a known volume ($5 - 10 \text{ mL}$) of cold or room-temperature saline through the proximal RA port and recording temperature change over time at the distal thermistor tip in the pulmonary artery:

$CO = \frac{V_i \cdot (T_b - T_i) \cdot K_1 \cdot K_2}{\int_0^\infty \Delta T_b(t) \, dt}$

• Area Under the Curve (AUC): Cardiac output is inversely proportional to the area under the thermodilution temperature-time curve:
  • High Cardiac Output: Rapid transit of blood $\to$ rapid washout of cold bolus $\to$ small AUC.
  • Low Cardiac Output: Slow transit of blood $\to$ delayed clearance of cold bolus $\to$ large, broad AUC.

+-------------------------------------------------------------------------+
|                   THERMODILUTION INACCURACY SCENARIOS                   |
+------------------------------------+------------------------------------+
| Error / Pathologic Condition       | Cardiac Output Calculation Effect  |
+------------------------------------+------------------------------------+
| **Severe Tricuspid Regurgitation** | • Falsely UNDERESTIMATES CO        |
|                                    | • Cold injectate regurgitates back |
|                                    |   and forth, prolonging washout    |
|                                    |   and artificially enlarging AUC   |
| **Injectate Volume LESS than set** | • Falsely OVERESTIMATES CO         |
|                                    | • Produces artificially small AUC  |
| **Injectate Volume GREATER set**   | • Falsely UNDERESTIMATES CO        |
| **Intracardiac Left-to-Right Shunt**| • Invalids thermodilution method   |
+------------------------------------+------------------------------------+

Mixed Venous Oxygen Saturation ($SvO_2$)

Mixed venous blood is sampled from the distal pulmonary artery port of a PAC (normal $SvO_2$: $65 - 75%$, $PvO_2 \approx 40 \text{ mmHg}$). Central venous oxygen saturation ($ScvO_2$) drawn from an internal jugular CVP line is normally $70 - 80%$ (approximately $3 - 5%$ higher than $SvO_2$).

$SvO_2 = SaO_2 - \frac{VO_2}{CO \cdot 1.34 \cdot [Hb] \cdot 10}$

+-------------------------------------------------------------------------+
|                       SvO₂ CLINICAL ALTERATIONS                         |
+------------------------------------+------------------------------------+
| Decreased SvO₂ (< 65%)             | Increased SvO₂ (> 75-80%)          |
| (Increased extraction / low supply)| (Decreased extraction / excess sup)|
+------------------------------------+------------------------------------+
| • Decreased Cardiac Output (shock) | • Severe Sepsis / Endotoxemia      |
| • Arterial Hypoxemia (low SaO₂)    |   (microvascular AV shunting)      |
| • Anemia / Severe Hemorrhage       | • Cyanide Poisoning / Met-Hb       |
| • Hyperthermia, Shivering, Seizures|   (cellular histotoxic poisoning)  |
| • Malignant Hyperthermia           | • Hypothermia (reduced VO₂)        |
| • Thyroid Storm                    | • Wedged PAC (measures capillary)  |
+------------------------------------+------------------------------------+