2.3 Hemodynamic Profiling and Invasive Hemodynamics

Q: An acute care nurse evaluates a patient admitted with acute decompensated heart failure who is dyspneic at rest with bibasilar crackles, 3+ bilateral lower extremity edema, and a JVP of 6 cm above the sternal angle. The patient's extremities are warm to the touch, capillary refill is 1.5 seconds, blood pressure is 142/88 mmHg, and urine output is 65 mL/h. Which Stevenson hemodynamic profile does this patient exhibit, and what is the first-line pharmacotherapy?

Profile B ("Warm and Wet"); administer intravenous loop diuretics and consider intravenous vasodilators.. This patient exhibits signs of systemic and pulmonary venous congestion (dyspnea, bibasilar rales, 3+ peripheral edema, elevated JVP) combined with evidence of adequate peripheral perfusion (warm extremities, brisk capillary refill 0.5 mL/kg/h). This presentation defines Stevenson Profile B ("Warm and Wet"), which accounts for roughly 65% to 70% of acute heart failure admissions. The frontline management for Profile B is aggressive intravenous loop diuresis to achieve decongestion, often accompanied by intravenous vasodilators (such as nitroglycerin or nitroprusside) if blood pressure permits, to rapidly reduce ventricular preload and afterload. Profile A ("Warm and Dry") describes a compensated patient without congestion or hypoperfusion. Profile L ("Cold and Dry") describes a hypoperfused patient without congestion, for whom a cautious fluid challenge is appropriate. Profile C ("Cold and Wet") represents cardiogenic shock characterized by cold, hypoperfused extremities, narrow pulse pressure, and end-organ dysfunction requiring inotropes or mechanical circulatory support.

Q: A patient in the cardiac intensive care unit with acute cardiogenic shock secondary to severe ischemic cardiomyopathy has a pulmonary artery catheter in place. The nurse records the following measurements: Mean Arterial Pressure (MAP) 65 mmHg, Right Atrial Pressure (RAP) 14 mmHg, Pulmonary Capillary Wedge Pressure (PCWP) 22 mmHg, Cardiac Output (CO) 3.2 L/min, Body Surface Area (BSA) 2.0 m2, and Mixed Venous Oxygen Saturation (SvO2) 48%. What do the calculated Cardiac Index (CI), Systemic Vascular Resistance (SVR), and SvO2 reveal about the patient's hemodynamic state?

CI 1.6 L/min/m2, SVR 1275 dynes·s/cm5, SvO2 48%; cardiogenic shock with elevated filling pressures, compensatory vasoconstriction, and high tissue oxygen extraction.. Cardiac Index is calculated as Cardiac Output divided by BSA: 3.2 L/min / 2.0 m2 = 1.6 L/min/m2 (normal: 2.5 to 4.0 L/min/m2), which is well below the cardiogenic shock threshold of 2.2 L/min/m2. Systemic Vascular Resistance is calculated as [(MAP - RAP) / CO] × 80: [(65 - 14) / 3.2] × 80 = (51 / 3.2) × 80 = 15.9375 × 80 = 1275 dynes·s/cm5 (normal: 800 to 1200 dynes·s/cm5), reflecting compensatory neurohormonal vasoconstriction. The PCWP of 22 mmHg confirms severe pulmonary capillary congestion (normal: 6 to 12 mmHg). The SvO2 of 48% is critically reduced (normal: 65% to 75%), demonstrating that peripheral tissues are extracting a markedly increased fraction of delivered oxygen to compensate for the severely depressed systemic blood flow. Classifying this profile as distributive septic shock is incorrect because septic shock features low SVR (< 800) and typically elevated CI and SvO2. Claiming normal cardiac performance ignores the profoundly depressed CI of 1.6 L/min/m2. Suggesting volume depletion contradicts the elevated filling pressures (RAP 14 mmHg and PCWP 22 mmHg).

Q: A 52-year-old female with end-stage non-ischemic cardiomyopathy is undergoing evaluation for orthotopic heart transplantation. Baseline right heart catheterization reveals a mean Pulmonary Artery Pressure (mPAP) of 38 mmHg, a PCWP of 18 mmHg, and a Cardiac Output of 4.0 L/min. During inhaled nitric oxide testing, mPAP decreases to 24 mmHg, PCWP remains 16 mmHg, and CO increases to 4.5 L/min. How should the heart failure team interpret the baseline and vasodilator Pulmonary Vascular Resistance (PVR)?

Baseline PVR is 5.0 Wood units (elevated), which successfully reverses to approximately 1.8 Wood units with pulmonary vasodilation, confirming acceptable risk for isolated heart transplantation.. Pulmonary Vascular Resistance in Wood units is calculated as (mean PAP - PCWP) / Cardiac Output. At baseline: (38 - 18) / 4.0 = 20 / 4.0 = 5.0 Wood units. Normal PVR is less than 2 Wood units; values above 3 to 5 Wood units indicate significant pulmonary hypertension. A fixed, unresponsive PVR > 3 to 5 Wood units is a major contraindication to isolated heart transplantation because the unconditioned donor right ventricle cannot overcome high pulmonary pressures and will fail acutely post-transplant. During inhaled nitric oxide vasodilator challenge, the patient's PVR becomes: (24 - 16) / 4.5 = 8 / 4.5 ≈ 1.78 Wood units. Because the PVR drops below 2 to 2.5 Wood units in response to a selective pulmonary vasodilator, the pulmonary hypertension is demonstrated to be reversible (reactive rather than fixed vascular remodeling), confirming that the patient is a viable candidate for heart transplantation. Calculating baseline PVR as 1.0 Wood unit errors in the subtraction of PCWP from mPAP. Stating that PVR was unresponsive contradicts the documented drop to ~1.8 Wood units. Reporting 20 Wood units mistakes the transpulmonary pressure gradient (20 mmHg) for the calculated vascular resistance.

Key Takeaways

The Stevenson 2×2 hemodynamic matrix categorizes acute heart failure into four clinical profiles based on volume/congestion (Wet vs Dry; PCWP threshold 18 mmHg) and systemic perfusion (Warm vs Cold; Cardiac Index threshold 2.2 L/min/m2).
Profile B ('Warm and Wet') is the most common presentation of acute decompensated heart failure (~65–70% of admissions); treatment requires intravenous loop diuretics and preload/afterload-reducing vasodilators.
Profile C ('Cold and Wet') represents decompensated cardiogenic shock; management requires urgent inotropic support (dobutamine or milrinone) or temporary mechanical circulatory support before aggressive diuresis can be safely initiated.
Normal resting invasive hemodynamic parameters are: RAP 2–6 mmHg, PAP 20–30 / 8–12 mmHg, PCWP 6–12 mmHg, Cardiac Index 2.5–4.0 L/min/m2, and SVR 800–1200 dynes·s/cm5.
Mixed venous oxygen saturation (SvO2), measured from the distal pulmonary artery, normally ranges from 65% to 75%; an SvO2 < 60% indicates excessive peripheral tissue oxygen extraction secondary to inadequate forward cardiac output.

Last updated: September 2026

Hemodynamic Profiling and Invasive Hemodynamics

Precise hemodynamic assessment is fundamental to the evaluation and management of acute decompensated heart failure (ADHF) and cardiogenic shock. Clinicians must rapidly determine two physiological dimensions: volume/congestion status (left and right ventricular filling pressures) and systemic perfusion status (forward cardiac output and end-organ delivery). While non-invasive bedside examination provides rapid clinical categorization, invasive hemodynamic monitoring via right heart catheterization (RHC / pulmonary artery catheter / Swan-Ganz) offers precise quantitative data to guide advanced medical and mechanical therapies.

The Clinical 2×2 Hemodynamic Matrix: Stevenson & Forrester Frameworks

Originally developed by Forrester for post-myocardial infarction shock and later adapted by Lynne Stevenson for bedside evaluation of chronic and acute heart failure, the 2×2 Hemodynamic Matrix categorizes patients into four distinct clinical profiles based on the presence or absence of congestion ('Wet' vs 'Dry') and hypoperfusion ('Cold' vs 'Warm').

                             PERFUSION STATUS
                   Warm (Adequate)           Cold (Hypoperfused)
               (CI > 2.2 L/min/m2)          (CI <= 2.2 L/min/m2)
           +--------------------------+--------------------------+
           |                          |                          |
    Dry    |        PROFILE A         |        PROFILE L         |
(Euvolemic)|      'Warm and Dry'      |      'Cold and Dry'      |
 PCWP <= 18|  - Compensated, stable  |  - Overdiuresed / lean   |
   mmHg    |  - Outpatient GDMT       |  - Cautious fluid trial  |
           |                          |                          |
CONGESTION +--------------------------+--------------------------+
  STATUS   |                          |                          |
    Wet    |        PROFILE B         |        PROFILE C         |
(Congested)|      'Warm and Wet'      |      'Cold and Wet'      |
 PCWP > 18 |  - 65-70% of admissions  |  - Cardiogenic shock     |
   mmHg    |  - IV Loop Diuretics     |  - Inotropes, pressors,  |
           |  - IV Vasodilators       |    MCS, diuresis later   |
           +--------------------------+--------------------------+

The Four Profiles: Assessment and Emergency Management

Profile	Clinical Quadrant	Hemodynamic Criteria	Clinical Signs & Symptoms	Immediate Nursing & Medical Priorities
Profile A	Warm and Dry	CI > 2.2 L/min/m²; PCWP ≤ 18 mmHg	Euvolemic, warm extremities, normal pulses, no orthopnea, normal JVP (≤ 3 cm), no crackles, no edema.	Baseline target. Optimize and titrate guideline-directed medical therapy (GDMT: ARNI, beta-blocker, MRA, SGLT2i).
Profile B	Warm and Wet	CI > 2.2 L/min/m²; PCWP > 18 mmHg	Adequate perfusion with severe congestion: warm skin, normal pulse pressure, dyspnea, orthopnea, crackles, elevated JVP, positive AJR, peripheral edema. Most common ADHF presentation (~65–70%).	Decongestion: Administer intravenous loop diuretics (furosemide, bumetanide). Add IV vasodilators (nitroglycerin, nitroprusside) if blood pressure permits (SBP > 110 mmHg) to rapidly unload the ventricle.
Profile C	Cold and Wet	CI ≤ 2.2 L/min/m²; PCWP > 18 mmHg	Combined congestion and hypoperfusion: cool, clammy extremities, narrow pulse pressure (< 25 mmHg), oliguria, elevated JVP, crackles, S3 gallop, lactic acidosis. Cardiogenic shock.	Perfusion Restoration First: Administer inotropic infusions (dobutamine, milrinone). Add vasopressors (norepinephrine) if MAP < 65 mmHg. Escalate to temporary mechanical circulatory support (Impella, IABP). Avoid pure beta-blocker escalation. Cautious diuresis once perfusion is stabilized.
Profile L	Cold and Dry	CI ≤ 2.2 L/min/m²; PCWP ≤ 18 mmHg	Hypoperfusion without congestion ('L' for Low-output or Lean): cool extremities, narrow pulse pressure, fatigue, postural hypotension, low JVP, clear lungs, no edema, rising BUN/creatinine.	Re-evaluation & Volume Challenge: Suspend diuretics. If overdiuresed, administer a cautious crystalloid fluid challenge (250 to 500 mL) under close hemodynamic observation. If filling pressures rise without perfusion improvement, consider inotropes.

Right Heart Catheterization (RHC / Pulmonary Artery Catheter)

While non-invasive examination categorizes most heart failure presentations, invasive hemodynamic monitoring via a pulmonary artery catheter (PAC / Swan-Ganz) is indicated when diagnostic or therapeutic uncertainty persists.

Clinical Indications for RHC

Cardiogenic shock of uncertain or mixed etiology (e.g., differentiating cardiogenic shock from septic or vasodilatory shock).
Persistent hemodynamic instability refractory to initial empirical inotropes, vasopressors, or diuretics.
Guiding titration of complex vasoactive infusions and mechanical circulatory support devices (MCS).
Evaluation of pulmonary hypertension and right heart function for heart transplantation or left ventricular assist device (LVAD) candidacy.
Preoperative hemodynamic optimization in high-risk cardiac surgery.

[Introducer Sheath: Internal Jugular / Subclavian Vein]
                     |
                     v
[Right Atrial Port] --------------> RAP / CVP (Normal: 2-6 mmHg)
                     |
                     v  [Tricuspid Valve]
[Right Ventricle] ----------------> RVP (Systolic: 20-30 mmHg, Diastolic: 0-5 mmHg)
                     |
                     v  [Pulmonic Valve]
[Pulmonary Artery Distal Port] ---> PAP (Systolic: 20-30 mmHg, Diastolic: 8-12 mmHg)
                     |
                     v  [Balloon Inflated: Wedged in Capillary Branch]
[Wedge Position] -----------------> PCWP / PAOP (Normal: 6-12 mmHg; reflects LVEDP)

Invasive Hemodynamic Parameters, Reference Ranges, and Waveform Interpretation

Parameter	Abbreviation	Normal Range	Primary Clinical Interpretation in Heart Failure
Right Atrial Pressure	RAP / CVP	2 to 6 mmHg (3 to 8 cm H₂O)	Measures RV preload. Elevated (> 8–10 mmHg) in RV failure, tricuspid regurgitation, volume overload, and constrictive pericarditis.
Right Ventricular Pressure	RVP	Systolic: 20 to 30 mmHg; End-Diastolic: 0 to 5 mmHg	Elevated systolic in pulmonary hypertension; elevated diastolic in RV volume overload or failure.
Pulmonary Artery Pressure	PAP	Systolic: 20 to 30 mmHg; Diastolic: 8 to 12 mmHg; Mean: 10 to 20 mmHg	Mean PAP > 20 mmHg at rest defines pulmonary hypertension. Elevated diastolic indicates elevated downstream left-sided filling pressures or pulmonary vascular disease.
Pulmonary Capillary Wedge Pressure	PCWP / PAOP	6 to 12 mmHg	Measures pulmonary capillary pressure; directly reflects left atrial pressure (LAP) and left ventricular end-diastolic pressure (LVEDP) in the absence of mitral stenosis. Congestion threshold > 18 mmHg; hydrostatic pulmonary edema ensues when PCWP > 20–25 mmHg.
Cardiac Output	CO	4.0 to 8.0 L/min	Total forward volume of blood pumped per minute. Measured via thermodilution or Fick method.
Cardiac Index	CI	2.5 to 4.0 L/min/m²	Cardiac output standardized to body surface area (CI = CO/BSA). Cardiogenic shock threshold: CI < 2.2 L/min/m² (< 1.8 L/min/m² without support).
Systemic Vascular Resistance	SVR	800 to 1200 dynes·s/cm⁵	Afterload faced by the left ventricle. Markedly elevated (> 1400–2000) in cardiogenic shock due to compensatory vasoconstriction; low (< 800) in septic/distributive shock.
Pulmonary Vascular Resistance	PVR	0.5 to 2.0 Wood units (< 160 dynes·s/cm⁵)	Resistance across the pulmonary circulation. Fixed elevation (> 3–5 Wood units) contraindicates isolated heart transplantation.
Mixed Venous Oxygen Saturation	SvO₂	65% to 75%	Sampled from distal PA port. Measures residual oxygen returning to the right heart. Values < 60% indicate tissue hypoperfusion and excessive oxygen extraction.

The End-Expiration Measurement Rule for PCWP

The Rule: Pulmonary Capillary Wedge Pressure and Pulmonary Artery Diastolic Pressure must always be measured at end-expiration.
Physiological Rationale: Respiration causes cyclical fluctuations in intrathoracic pressure. During spontaneous inspiration, intrathoracic pressure becomes negative, falsely lowering vascular pressures. At end-expiration, intrathoracic pressure is closest to atmospheric zero, ensuring that the transducer measures purely intravascular pressure.
Mechanical Ventilation Distinction: In positive-pressure mechanical ventilation, inspiration increases intrathoracic pressure, producing pressure peaks; end-expiration corresponds to the lowest point (trough) of the respiratory pressure waveform.

Thermodilution versus Indirect Fick Cardiac Output

Thermodilution Method: Relies on injecting a known volume of cold crystalloid into the right atrial port and measuring the downstream temperature curve at the distal thermistor.
- Pitfall: Inaccurate in patients with severe tricuspid regurgitation (the regurgitant jet washes the thermal indicator back and forth, falsely underestimating cardiac output) or severe low-flow states.
Indirect Fick Method: Calculates cardiac output based on oxygen consumption (VO₂) and the arteriovenous oxygen difference: CO = VO₂/((CaO₂ - CvO₂) × 10).
- Clinical Pearl: The Fick method is preferred in patients with severe tricuspid regurgitation, intracardiac shunts, or low-output cardiogenic shock.

Formula Calculations

$\text{CI} = \frac{\text{CO}}{\text{BSA}}$ $\text{SVR} = \frac{\text{MAP} - \text{RAP}}{\text{CO}} \times 80$ $\text{PVR (Wood units)} = \frac{\text{mean PAP} - \text{PCWP}}{\text{CO}}$ Note: To convert PVR from Wood units to dynes·s/cm⁵, multiply by 80.

Mixed Venous (SvO₂) versus Central Venous (ScvO₂) Oxygen Saturation

Mixed Venous (SvO₂): Drawn exclusively from the distal port of a pulmonary artery catheter, representing true mixed venous blood from the superior vena cava, inferior vena cava, and coronary sinus. Normal range is 65% to 75%.
Tissue Extraction Physiology: When cardiac output falls, systemic tissues extract a higher percentage of delivered oxygen, dropping the SvO₂ below 60%. If SvO₂ falls below 50%, tissue anaerobiosis and lactic acidosis ensue.
Central Venous Saturation (ScvO₂): Drawn from a central venous catheter tip in the superior vena cava (pre-right atrium). Normal ScvO₂ is 70% to 75%, running approximately 5% higher than SvO₂ because it lacks the highly desaturated venous effluent of the coronary sinus.

PVR Reversibility Testing in Cardiac Transplantation

In heart failure evaluation, elevated pulmonary pressures can reflect passive backward transmission of elevated left ventricular filling pressures (post-capillary pulmonary hypertension, defined by PCWP > 15 mmHg and PVR < 2–3 Wood units) or chronic pulmonary arteriolar remodeling (pre-capillary component).

If the baseline PVR is > 3 to 5 Wood units, the patient must undergo pharmacological vasodilator challenge (using inhaled nitric oxide, intravenous nitroprusside, or milrinone).
If the PVR drops below 3 Wood units without causing severe systemic hypotension, the pulmonary hypertension is deemed reversible, and the patient remains eligible for orthotopic heart transplantation.
If PVR remains fixed above 3 to 5 Wood units, the donor heart's unadapted right ventricle would face acute afterload mismatch and fail post-transplant, necessitating consideration of a durable left ventricular assist device (LVAD) to allow long-term unloading or combined heart-lung transplantation.

Clinical Case Scenario

A 61-year-old male with an acute anterior STEMI undergoes emergency percutaneous coronary intervention (PCI) with stenting of the LAD. After the procedure, in the cardiac ICU, he is oliguric (15 mL/h), confused, and cool to his mid-thighs. His blood pressure is 82/60 mmHg (MAP 67 mmHg), and heart rate is 104 bpm. A pulmonary artery catheter is placed, yielding the following measurements: RAP 15 mmHg, PAP 46/26 mmHg (mean PAP 33 mmHg), PCWP 24 mmHg (at end-expiration), CO 3.0 L/min, BSA 1.9 m², and distal PA SvO₂ 46%.

Hemodynamic Calculations & Profile:

CI = (3.0 L/min)/(1.9 m²) = 1.58 L/min/m² (Severely depressed; shock threshold < 2.2).
SVR = (67 - 15)/3.0 × 80 = 52/3.0 × 80 = 1387 dynes·s/cm⁵ (Markedly elevated compensatory vasoconstriction).
PVR = (33 - 24)/3.0 = 9/3.0 = 3.0 Wood units.
Profile: Profile C ("Cold and Wet") cardiogenic shock with elevated filling pressures (PCWP 24, RAP 15), severely depressed cardiac index (1.58), high SVR (1387), and intense tissue oxygen extraction (SvO₂ 46%).

Emergency Management: The nurse recognizes that immediate administration of an inotrope (dobutamine) or placement of a mechanical circulatory support device (such as an Impella microaxial pump) is required to restore forward perfusion. Diuretics alone would further drop stroke volume and precipitate cardiovascular collapse.

Test Your Knowledge

An acute care nurse evaluates a patient admitted with acute decompensated heart failure who is dyspneic at rest with bibasilar crackles, 3+ bilateral lower extremity edema, and a JVP of 6 cm above the sternal angle. The patient's extremities are warm to the touch, capillary refill is 1.5 seconds, blood pressure is 142/88 mmHg, and urine output is 65 mL/h. Which Stevenson hemodynamic profile does this patient exhibit, and what is the first-line pharmacotherapy?

Profile A ("Warm and Dry"); initiate high-dose dopamine infusion and discontinue all baseline beta-blockers.

Profile L ("Cold and Dry"); administer a 1,000 mL rapid crystalloid bolus followed by oral fluid loading.

Profile B ("Warm and Wet"); administer intravenous loop diuretics and consider intravenous vasodilators.

Profile C ("Cold and Wet"); initiate emergency mechanical circulatory support and hold all diuretic therapy.

Test Your Knowledge

A patient in the cardiac intensive care unit with acute cardiogenic shock secondary to severe ischemic cardiomyopathy has a pulmonary artery catheter in place. The nurse records the following measurements: Mean Arterial Pressure (MAP) 65 mmHg, Right Atrial Pressure (RAP) 14 mmHg, Pulmonary Capillary Wedge Pressure (PCWP) 22 mmHg, Cardiac Output (CO) 3.2 L/min, Body Surface Area (BSA) 2.0 m2, and Mixed Venous Oxygen Saturation (SvO2) 48%. What do the calculated Cardiac Index (CI), Systemic Vascular Resistance (SVR), and SvO2 reveal about the patient's hemodynamic state?

CI 2.8 L/min/m2, SVR 650 dynes·s/cm5, SvO2 48%; distributive septic shock with high cardiac output and pathological vasodilation.

CI 3.2 L/min/m2, SVR 1000 dynes·s/cm5, SvO2 48%; normal cardiac performance with isolated hypoxemic respiratory failure.

CI 1.6 L/min/m2, SVR 800 dynes·s/cm5, SvO2 48%; compensated volume depletion requiring immediate large-volume crystalloid resuscitation.

CI 1.6 L/min/m2, SVR 1275 dynes·s/cm5, SvO2 48%; cardiogenic shock with elevated filling pressures, compensatory vasoconstriction, and high tissue oxygen extraction.

Test Your Knowledge

A 52-year-old female with end-stage non-ischemic cardiomyopathy is undergoing evaluation for orthotopic heart transplantation. Baseline right heart catheterization reveals a mean Pulmonary Artery Pressure (mPAP) of 38 mmHg, a PCWP of 18 mmHg, and a Cardiac Output of 4.0 L/min. During inhaled nitric oxide testing, mPAP decreases to 24 mmHg, PCWP remains 16 mmHg, and CO increases to 4.5 L/min. How should the heart failure team interpret the baseline and vasodilator Pulmonary Vascular Resistance (PVR)?

Baseline PVR is 1.0 Wood unit, indicating completely normal pulmonary pressures that require no vasodilator testing.

Baseline PVR is 5.0 Wood units (elevated), which successfully reverses to approximately 1.8 Wood units with pulmonary vasodilation, confirming acceptable risk for isolated heart transplantation.

Baseline PVR is 8.5 Wood units and completely unresponsive to nitric oxide, representing a strict contraindication to any surgical intervention.

Baseline PVR is 20 Wood units, proving severe systemic vascular collapse that mandates emergency venoarterial ECMO.

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2.3 Hemodynamic Profiling and Invasive Hemodynamics

Key Takeaways

Hemodynamic Profiling and Invasive Hemodynamics

The Clinical 2×2 Hemodynamic Matrix: Stevenson & Forrester Frameworks

The Four Profiles: Assessment and Emergency Management

Right Heart Catheterization (RHC / Pulmonary Artery Catheter)

Clinical Indications for RHC

Invasive Hemodynamic Parameters, Reference Ranges, and Waveform Interpretation

The End-Expiration Measurement Rule for PCWP

Thermodilution versus Indirect Fick Cardiac Output

Formula Calculations

Mixed Venous (SvO₂) versus Central Venous (ScvO₂) Oxygen Saturation

PVR Reversibility Testing in Cardiac Transplantation

Clinical Case Scenario

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1Chapter 1: Patient History, Risk Factors, and Etiologies

2Chapter 2: Physical Examination and Hemodynamic Evaluation

3Chapter 3: Laboratory Biomarkers and Diagnostic Testing

4Chapter 4: Classification, Staging, and Functional Assessment

5Chapter 5: Individualized Care Planning and Shared Decision-Making

6Chapter 6: GDMT Pharmacotherapy for HFrEF

7Chapter 7: Diuretics, HFpEF, Comorbidity Pharmacotherapy, and Medication Safety

8Chapter 8: Device Therapy, Rhythm Management, and Advanced Interventions

9Chapter 9: Patient Education, Self-Care, Screening, and Referrals

10Chapter 10: Therapy Effectiveness, Monitoring, and Care Transitions

11Chapter 11: Patient Comprehension, Self-Care Adherence, and Palliative Transitions

12Chapter 12: Professional Standards, Ethics, Quality, and Certification

AAHFN CHFN Certified Heart Failure Nurse

2.3 Hemodynamic Profiling and Invasive Hemodynamics

Key Takeaways

Hemodynamic Profiling and Invasive Hemodynamics

The Clinical 2×2 Hemodynamic Matrix: Stevenson & Forrester Frameworks

The Four Profiles: Assessment and Emergency Management

Right Heart Catheterization (RHC / Pulmonary Artery Catheter)

Clinical Indications for RHC

Invasive Hemodynamic Parameters, Reference Ranges, and Waveform Interpretation

The End-Expiration Measurement Rule for PCWP

Thermodilution versus Indirect Fick Cardiac Output

Formula Calculations

Mixed Venous (SvO₂) versus Central Venous (ScvO₂) Oxygen Saturation

PVR Reversibility Testing in Cardiac Transplantation

Clinical Case Scenario