Hemodynamics – Invasive Monitoring Study Notes

General Principles

• Invasive monitoring is common in ICU for critically ill patients.

• Provides information on:

  • Hemodynamics

  • Response to treatments

  • Blood flow/perfusion changes

• Always correlate monitor values with patient condition.

  • Numbers may look good but patient unstable → investigate.

  • Numbers may look bad but patient clinically stable → interpret cautiously.

Central Venous Pressure (CVP)

• Definition: Pressure in right atrium → reflects right heart preload (venous return).

• Normal: 2–10 mmHg.

• Obtained via: Central venous catheter (central line).

• Waveform: Small oscillating waves.

• Causes of ↑ CVP:

  • Fluid overload

  • Cardiac tamponade

  • Right heart dysfunction/failure

• Causes of ↓ CVP:

  • Hypovolemia (dehydration, blood/fluid loss)

  • Venodilation → pooling of blood

Arterial Line (A-line)

• Definition: Catheter placed in artery (radial, femoral, brachial, pedal).

• Measures:

  • Systolic BP

  • Diastolic BP

  • MAP (mean arterial pressure)

• Advantages: Real-time, continuous BP (important for vasoactive drips).

• Waveform:

  • Upstroke = systolic

  • Dicrotic notch = aortic valve closure

  • Downstroke = diastolic

• Accuracy issues:

  • Underdamped (whip): High systolic, low diastolic, exaggerated peaks.

  • Overdamped (flat): Loss of notch, falsely low systolic, high diastolic.

• If waveform accurate: A-line values are more reliable than cuff BP.

FloTrac / Vigileo System (Edwards Lifesciences)

• Uses A-line tracing with proprietary transducer & monitor.

• Provides:

  1. Stroke Volume (SV) / Stroke Volume Index (SVI)

  2. Cardiac Output (CO) / Cardiac Index (CI)

  3. Stroke Volume Variation (SVV)

• Mechanism: Algorithm relates pulse pressure changes to stroke volume.

Stroke Volume Variation (SVV)

• Normal: <13%

• High SVV (>13%): Low preload/volume depletion → likely fluid responsive.

• Based on pulsus paradoxus: Greater variation in BP with ventilation = less volume.

• Limitations:

  • Inaccurate with spontaneous breathing, arrhythmias (esp. AFib), or open chest.

• Passive Leg Raise (PLR): Temporary “auto-bolus” → ↑ SV/CO suggests fluid responsive.

Pulmonary Artery Catheter (Swan-Ganz / PA Cath)

• Inserted via large vein → RA → RV → PA.

• Multiple ports for pressure readings and infusions.

Key Measurements

1. Right Atrial Pressure (CVP)

   • Normal: 2–10 mmHg.

2. Pulmonary Artery Pressure (PAP)

   • Normal: 20–30 / 10–20 mmHg.

   • ↑ Causes: Septal defect, pulmonary HTN, LV failure, mitral stenosis/regurgitation.

   • Think of PAP as the “A-line” of the right heart.

3. Pulmonary Capillary Wedge Pressure (PCWP / PAWP)

   • Obtained by inflating balloon → occludes PA branch.

   • Reflects left heart preload (LV filling pressure).

   • Normal: 8–12 mmHg.

   • ↑ PCWP: Fluid overload, LV failure, tamponade, mitral/aortic valve disease.

   • ↓ PCWP: Hypovolemia, vasodilation.

   • Balloon must be deflated after measurement → avoid pulmonary artery obstruction.

4. Cardiac Output (CO) / Cardiac Index (CI)

   • Measured continuously (most modern) or intermittently (older thermodilution).

Additional Parameters

• Systemic Vascular Resistance (SVR): 800–1200 dyn·s/cm⁵

  • ↓ (<800): Vasodilation, low resistance, hypotension.

  • ↑ (>1200): Vasoconstriction, ↑ afterload.

• Pulmonary Vascular Resistance (PVR): Reflects afterload on right ventricle.

• Some catheters measure SvO₂ (mixed venous oxygen sat).

Key Takeaways

• Always integrate invasive monitor readings with clinical assessment.

• CVP → right-sided preload.

• A-line → continuous BP, MAP, waveform quality essential.

• FloTrac → adds SV, CO/CI, SVV (fluid responsiveness).

• Swan-Ganz → comprehensive pressures (RA, PAP, PCWP), CO/CI, vascular resistance.

• Each tool has limitations; interpret in

•  context.

• Cardiac Output Study Notes

Cardiac Output (CO)

• Formula: CO = HR × SV

• Normal values:

  • Stroke Volume (SV): 60–120 mL/beat

  • Heart Rate (HR): 60–100 bpm

  • Cardiac Output (CO): 4–8 L/min

  • Cardiac Index (CI): 2.5–4 L/min/m²

Key principle: HR and SV work together in a seesaw manner:

• ↓ SV → ↑ HR (compensation)

• ↑ SV → ↓ HR (compensation)

Heart Rate (HR)

• Primary role: Compensates for changes in stroke volume.

Tachycardia (>100 bpm)

• Causes:

  • Hypovolemia (dehydration, blood loss, fluid loss)

  • Hypotension

  • Sympathetic stimulation (catecholamines: fight/flight)

  • Fever

  • Exercise

• Limitations:

  • Healthy heart: >180 bpm → inadequate filling time → ↓ CO

  • Diseased/deconditioned heart: >120 bpm already harmful

Bradycardia (<60 bpm)

• Common in athletes (strong SV, efficient contraction).

• Often benign if patient asymptomatic.

Arrhythmias and Conduction Issues

• Atrial fibrillation/flutter: Loss of atrial kick → ↓ preload & CO

• Junctional/idioventricular rhythms: Slow HR → ↓ CO

• Heart blocks (2nd/3rd degree): Impaired HR control → ↓ CO

• MI: Can impair conduction and HR regulation

• Medications: Beta-blockers, calcium channel blockers blunt HR response

Stroke Volume (SV)

• Formula: SV is determined by:

  • Preload

  • Contractility

  • Afterload

1. Contractility

• Definition: Squeeze/force of ventricular contraction.

• ↑ Contractility → ↑ SV → ↑ O₂ demand

• ↓ Contractility → ↓ SV → ↓ O₂ demand

Increased by: Sympathetic stimulation, exercise
Decreased by: MI, cardiac surgery, hypoxia, hypercapnia, hyperkalemia, hypocalcemia, metabolic acidosis

2. Preload

• Definition: Ventricular filling pressure = “how full the tank is”

• Influenced by:

  • Blood volume (absolute amount)

  • Fluid distribution (intravascular vs intracellular vs third spacing)

  • Atrial contraction (atrial kick = up to 20% of SV; lost in AF/flutter)

Frank-Starling Law:

• ↑ Preload → ↑ stretch of myocardium → stronger contraction (up to a point).

• Overstretching (↑ compliance): CHF, dilated cardiomyopathy → weak contraction.

• ↓ Compliance: MI, restrictive cardiomyopathy, stunned myocardium → stiff ventricle, poor filling.

3. Afterload

• Definition: Resistance the ventricle must overcome to eject blood (“how clamped down the vessels are”).

Determinants:

1. Aortic compliance – stiff aorta = ↑ afterload

2. Vascular resistance – vasoconstriction/narrow vessels ↑ resistance

   • Hypoxia can ↑ pulmonary vascular resistance

3. Blood viscosity – thicker blood (polycythemia) ↑ afterload; thinner blood ↓ afterload

Summary

• Cardiac Output = HR × SV

• HR and SV compensate for each other, but only within physiologic limits.

• SV is determined by contractility, preload, and afterload.

• Clinical implications:

  • Tachycardia may help temporarily but becomes harmful at high rates.

  • Arrhythmias and conduction blocks directly reduce CO.

  • Preload follows Frank-Starling but has limits in CHF.

  • Contractility and afterload directly shape SV and O₂ demand.