📋 Key Information Summary
- Cardiac output (CO) = heart rate (HR) × stroke volume (SV); normal resting CO in adults is 4–8 L/min, cardiac index (CI) 2.5–4.0 L/min/m².
- Stroke volume is determined by preload, afterload, and myocardial contractility (the three determinants of SV).
- Ejection fraction (EF) = (EDV − ESV) / EDV × 100; normal EF ≥ 55%; HF with reduced EF (HFrEF) defined as EF < 40%.
- Fractional shortening (FS) = (LVIDd − LVIDs) / LVIDd × 100; normal FS 25–45%; assessed on M-mode echocardiography.
- The Fick principle states CO = VO₂ / (CaO₂ − CvO₂), used as the gold-standard invasive CO measurement.
- Mean arterial pressure (MAP) = DBP + ⅓(SBP − DBP); target MAP ≥ 65 mmHg in most critically ill patients.
- Systemic vascular resistance (SVR) = 80 × (MAP − RAP) / CO; normal SVR 800–1200 dyne·s/cm⁵.
- Pulmonary vascular resistance (PVR) = 80 × (MPAP − PCWP) / CO; normal PVR < 250 dyne·s/cm⁵.
- Stroke work (SW) = SV × (MAP − PCWP) × 0.0136; quantifies left ventricular energy expenditure per beat.
- Cardiac power output (CPO) = MAP × CO / 451; CPO < 0.6 W in cardiogenic shock is a critical prognostic threshold.
- Pressure–velocity relationships and ventriculo-arterial coupling (Ees/Ea ratio ~1.0) are central to understanding cardiac efficiency.
- All formulas assume steady-state haemodynamics; dynamic values require integration over the full cardiac cycle for accuracy.
- Invasive haemodynamic monitoring (pulmonary artery catheter) remains the reference standard for direct Fick CO measurement in Australian tertiary centres.
Introduction & Australian Context
Understanding cardiac physiology — encompassing pressure–velocity relationships, cardiac output, ejection fraction, and the Fick principle — is foundational for cardiologists, intensivists, and general physicians managing haemodynamic compromise in Australian clinical practice. These parameters underpin the diagnosis, severity assessment, and treatment of heart failure, cardiogenic shock, valvular disease, and pulmonary hypertension.
Heart failure affects an estimated 480,000 Australians, with a prevalence rising steeply with age — approximately 15% in those aged ≥ 85 years. Hospitalisation for acute decompensated heart failure represents one of the most common causes of medical admission in Australian tertiary hospitals, with the AIHW reporting over 69,000 heart failure-related separations annually. Mortality at one year following a first admission remains approximately 30%, underscoring the importance of precise haemodynamic assessment and timely intervention.
This guideline provides a comprehensive, formula-driven reference for the core parameters used in cardiac physiology, with emphasis on measurement techniques available in Australian centres, normal ranges, clinical interpretation, and integration with contemporary echocardiographic and invasive monitoring modalities.
Cardiac Output, Stroke Volume & Heart Rate
Core Definitions
Cardiac output (CO) is the volume of blood pumped by each ventricle per minute and is the product of heart rate and stroke volume:
CO = HR × SV
where CO = cardiac output (L/min), HR = heart rate (beats/min), SV = stroke volume (mL/beat).
Normal resting CO: 4–8 L/min (adult)
where CO = cardiac output (L/min), HR = heart rate (beats/min), SV = stroke volume (mL/beat).
Normal resting CO: 4–8 L/min (adult)
Cardiac Index
Because CO varies with body size, cardiac index (CI) normalises output to body surface area (BSA):
CI = CO / BSA
Normal CI: 2.5–4.0 L/min/m²
Normal CI: 2.5–4.0 L/min/m²
Body surface area is most commonly estimated using the Dubois formula: BSA (m²) = 0.007184 × Height(cm)0.725 × Weight(kg)0.425. The Mosteller formula (BSA = √(Height × Weight / 3600)) provides a rapid bedside estimate.
Stroke Volume
Stroke volume is the volume of blood ejected per ventricular contraction. Normal resting SV is 60–100 mL/beat. Stroke volume is governed by three interdependent determinants:
Determinant 1
Preload
End-diastolic fibre length; clinically approximated by left ventricular end-diastolic volume (LVEDV) or pressure (LVEDP/PCWP). Governed by the Frank–Starling mechanism.
↑ preload → ↑ SV (to a physiological limit)
Determinant 2
Afterload
Resistance against which the ventricle must eject; left ventricular afterload is approximated by systemic vascular resistance (SVR) and aortic impedance.
↑ afterload → ↓ SV (in a failing ventricle)
Determinant 3
Contractility
Intrinsic myocardial performance independent of loading conditions; indexed by Ees (end-systolic elastance). Influenced by sympathetic tone, inotropes, ischaemia.
↑ contractility → ↑ SV at any given preload
Stroke Volume Index
SVI = SV / BSA
Normal SVI: 33–47 mL/m²/beat
Normal SVI: 33–47 mL/m²/beat
Heart Rate Regulation
Normal resting adult heart rate: 60–100 bpm. The sinoatrial (SA) node intrinsic rate is approximately 100 bpm, modulated by:
- Sympathetic stimulation: β₁-adrenergic → ↑ HR (chronotropy), ↑ contractility (inotropy), ↑ conduction velocity (dromotropy).
- Parasympathetic (vagal) stimulation: M₂ muscarinic → ↓ HR, ↓ AV conduction.
- Intrinsic factors: stretch, catecholamines, temperature, electrolytes (K⁺, Ca²⁺).
Clinical note: Tachycardia (HR > 100 bpm) may initially maintain CO when SV falls, but excessive tachycardia reduces ventricular filling time and impairs diastolic coronary perfusion, ultimately worsening cardiac output. Heart rates > 150 bpm in the context of structural heart disease frequently precipitate haemodynamic collapse.
Pressure–Velocity Relationships & the Fick Principle
The Fick Principle
Adolf Fick (1870) described that the uptake or release of a substance by an organ equals the arteriovenous difference of that substance multiplied by blood flow. Applied to oxygen:
CO = VO₂ / (CaO₂ − CvO₂)
VO₂ = oxygen consumption (mL O₂/min), typically ~250 mL/min at rest in a 70 kg adult.
CaO₂ = arterial oxygen content (mL O₂/dL blood)
CvO₂ = mixed venous oxygen content (mL O₂/dL blood)
Oxygen content = (1.34 × Hb × SaO₂) + (0.003 × PaO₂)
VO₂ = oxygen consumption (mL O₂/min), typically ~250 mL/min at rest in a 70 kg adult.
CaO₂ = arterial oxygen content (mL O₂/dL blood)
CvO₂ = mixed venous oxygen content (mL O₂/dL blood)
Oxygen content = (1.34 × Hb × SaO₂) + (0.003 × PaO₂)
Deriving CaO₂ and CvO₂
| Parameter | Formula | Normal Value |
|---|---|---|
| CaO₂ (arterial O₂ content) | (1.34 × Hb × SaO₂) + (0.003 × PaO₂) | 16–20 mL O₂/dL |
| CvO₂ (mixed venous O₂ content) | (1.34 × Hb × SvO₂) + (0.003 × PvO₂) | 12–15 mL O₂/dL |
| CaO₂ − CvO₂ (a-v O₂ difference) | — | 3.5–5.5 mL O₂/dL |
| Oxygen delivery (DO₂) | CO × CaO₂ × 10 | 900–1100 mL O₂/min |
| Oxygen extraction ratio (O₂ER) | (CaO₂ − CvO₂) / CaO₂ | 0.22–0.30 (22–30%) |
Assumption caveat: The direct Fick method assumes steady-state VO₂, which is difficult to maintain in an acutely unwell patient. Indirect calorimetry (metabolic cart) provides the most accurate VO₂ measurement; estimated VO₂ (125 mL/min/m² × BSA, or 3.5 mL/kg/min) introduces up to 15–20% error.
Measurement in Australian Centres
Direct Fick CO measurement requires:
- Pulmonary artery catheter (Swan–Ganz) for mixed venous sampling (SvO₂ from PA port).
- Arterial blood gas or arterial line sampling for SaO₂/PaO₂.
- Metabolic cart for VO₂ (available in all Level 6 ICUs in Australia).
In practice, the thermodilution method (injectate-based or continuous) is more commonly used at the bedside in Australian tertiary ICUs and cardiac catheterisation laboratories, as it does not require VO₂ measurement. However, thermodilution remains calibrated against the Fick principle and is unreliable in the presence of significant tricuspid regurgitation or intracardiac shunts.
Pressure–Velocity Relationships
The relationship between ventricular pressure development and ejection velocity characterises myocardial performance. Key concepts include:
- dP/dtmax: Maximum rate of pressure rise during isovolumetric contraction; normally > 1200 mmHg/s. Reduced in systolic dysfunction; measured invasively or estimated from mitral regurgitation jet on Doppler echocardiography.
- Vmax: Theoretical maximum velocity of shortening at zero load; an index of contractility.
- Vcf (velocity of circumferential fibre shortening): Vcf = (LVIDd − LVIDs) / (LVIDd × ET), where ET = ejection time. Corrected Vcf (Vcfc) adjusts for heart rate.
Ventriculo-Arterial Coupling
Optimal cardiac efficiency occurs when ventricular elastance (Ees) is approximately equal to arterial elastance (Ea):
Ea = ESP / SV (end-systolic pressure / stroke volume)
Ees = ESP / ESV (end-systolic pressure / end-systolic volume)
Optimal coupling: Ees / Ea ≈ 1.0 (range 0.6–1.2)
Decoupling (Ees/Ea < 0.6) → impaired cardiac efficiency, seen in advanced systolic heart failure.
Ees = ESP / ESV (end-systolic pressure / end-systolic volume)
Optimal coupling: Ees / Ea ≈ 1.0 (range 0.6–1.2)
Decoupling (Ees/Ea < 0.6) → impaired cardiac efficiency, seen in advanced systolic heart failure.
Ejection Fraction & Fractional Shortening
Ejection Fraction (EF)
Ejection fraction is the most widely used clinical measure of left ventricular systolic function. It represents the proportion of end-diastolic volume ejected per beat:
EF = (EDV − ESV) / EDV × 100%
Equivalently: EF = SV / EDV × 100%
Normal EF: ≥ 55%
EDV = end-diastolic volume (normal ~120 mL)
ESV = end-systolic volume (normal ~50 mL)
SV = EDV − ESV (normal ~70 mL)
Equivalently: EF = SV / EDV × 100%
Normal EF: ≥ 55%
EDV = end-diastolic volume (normal ~120 mL)
ESV = end-systolic volume (normal ~50 mL)
SV = EDV − ESV (normal ~70 mL)
Heart Failure Classification by EF
HFrEF
EF < 40%
Heart failure with reduced ejection fraction. Neurohormonal activation predominates. Guideline-directed medical therapy (GDMT) has strongest evidence base.
Sacubitril/valsartan, beta-blockers, MRA, SGLT2i
HFmrEF
EF 40–49%
Heart failure with mildly reduced ejection fraction. Emerging evidence supports GDMT; individualised approach recommended.
Consider GDMT per HFrEF protocols
HFpEF
EF ≥ 50%
Heart failure with preserved ejection fraction. Diastolic dysfunction, impaired relaxation, and increased filling pressures. SGLT2 inhibitors show mortality benefit.
Empagliflozin, diuretics, manage comorbidities
Measurement Methods
| Modality | Method | Accuracy | Australian Availability |
|---|---|---|---|
| Transthoracic Echo (TTE) | Simpson's biplane (MOD) | Good (± 10%) | All hospitals; MBS item 55117 |
| CMR (Cardiac MRI) | Cine SSFP volumetric | Gold standard (± 5%) | Tertiary centres; MBS item 63339 |
| Nuclear (MUGA/RNVG) | Gated blood pool | Excellent (± 3–5%) | Selected centres; MBS item 61314 |
| CT angiography | Retrospective gating | Good | Widely available |
| Invasive angiography | Ventriculography | Moderate (foreshortening) | Cath labs |
Fractional Shortening (FS)
Fractional shortening is a one-dimensional (linear) surrogate for ejection fraction, measured by M-mode echocardiography at the level of the papillary muscles:
FS = (LVIDd − LVIDs) / LVIDd × 100%
LVIDd = left ventricular internal dimension in diastole (normal 3.9–5.3 cm)
LVIDs = left ventricular internal dimension in systole (normal 2.0–4.0 cm)
Normal FS: 25–45%
LVIDd = left ventricular internal dimension in diastole (normal 3.9–5.3 cm)
LVIDs = left ventricular internal dimension in systole (normal 2.0–4.0 cm)
Normal FS: 25–45%
Limitations of FS: Fractional shortening assumes symmetrical LV contraction and does not account for regional wall motion abnormalities. It significantly overestimates systolic function in dilated ventricles and underestimates it in concentric hypertrophy. EF by Simpson's biplane method is preferred for clinical decision-making. FS remains useful in paediatric echocardiography and serial follow-up of specific conditions.
Relationship Between EF and FS
Under the assumption of a prolate ellipsoid geometry, EF and FS are related by the cube function:
EF ≈ 1 − (1 − FS)³
For FS = 35%: EF ≈ 1 − 0.65³ ≈ 1 − 0.274 ≈ 73%
For FS = 25%: EF ≈ 1 − 0.75³ ≈ 1 − 0.422 ≈ 58%
This relationship degrades with abnormal geometry (e.g., aneurysm, asymmetric hypertrophy).
For FS = 35%: EF ≈ 1 − 0.65³ ≈ 1 − 0.274 ≈ 73%
For FS = 25%: EF ≈ 1 − 0.75³ ≈ 1 − 0.422 ≈ 58%
This relationship degrades with abnormal geometry (e.g., aneurysm, asymmetric hypertrophy).
Haemodynamic Parameters
Pressure Parameters
| Parameter | Formula / Definition | Normal Range |
|---|---|---|
| Mean Arterial Pressure (MAP) | MAP = DBP + ⅓(SBP − DBP) | 70–105 mmHg |
| Pulse Pressure (PP) | PP = SBP − DBP | 30–50 mmHg |
| Right Atrial Pressure (RAP) | CVP (central venous pressure) | 2–8 mmHg |
| Pulmonary Artery Systolic (PASP) | Invasive PA catheter / echo estimate | 15–30 mmHg |
| Mean PA Pressure (MPAP) | ⅓(PASP) + ⅔(PADP) | 9–18 mmHg |
| Pulmonary Capillary Wedge Pressure (PCWP) | Reflects LA/LVEDP | 6–12 mmHg |
| Left Ventricular End-Diastolic Pressure (LVEDP) | Invasive measurement | 5–12 mmHg |
Resistance Parameters
Systemic Vascular Resistance (SVR)
SVR = 80 × (MAP − RAP) / CO
Normal SVR: 800–1200 dyne·s/cm⁵
SVR units Wood units: (MAP − RAP) / CO = 10–20 WU
Pulmonary Vascular Resistance (PVR)
PVR = 80 × (MPAP − PCWP) / CO
Normal PVR: < 250 dyne·s/cm⁵
PVR in Wood units: (MPAP − PCWP) / CO = 0.25–2.5 WU
SVR = 80 × (MAP − RAP) / CO
Normal SVR: 800–1200 dyne·s/cm⁵
SVR units Wood units: (MAP − RAP) / CO = 10–20 WU
Pulmonary Vascular Resistance (PVR)
PVR = 80 × (MPAP − PCWP) / CO
Normal PVR: < 250 dyne·s/cm⁵
PVR in Wood units: (MPAP − PCWP) / CO = 0.25–2.5 WU
Pulmonary hypertension threshold: Mean PAP > 20 mmHg at rest (revised 6th WPHP, 2018). Pre-capillary PH additionally requires PVR > 3 Wood units and PCWP ≤ 15 mmHg. This replaces the older threshold of mPAP ≥ 25 mmHg.
Derived Work and Power Parameters
| Parameter | Formula | Normal / Interpretation |
|---|---|---|
| Stroke Work (SW) | SW = SV × (MAP − PCWP) × 0.0136 | Normal LVSW: 5–10 g·m/beat |
| Stroke Work Index (SWI) | SWI = SVI × (MAP − PCWP) × 0.0136 | Normal LVSWI: 40–60 g·m/m² |
| Cardiac Power Output (CPO) | CPO = (MAP × CO) / 451 | Normal: 1.0–1.7 W |
| Cardiac Power Index (CPI) | CPI = (MAP × CI) / 451 | Normal: 0.54–0.79 W/m² |
| Rate-Pressure Product (RPP) | RPP = HR × SBP | Index of myocardial O₂ demand; target < 20,000 at peak exercise |
Cardiogenic shock threshold: A cardiac power output (CPO) < 0.6 W at the time of presentation with cardiogenic shock is one of the strongest haemodynamic predictors of in-hospital mortality. Consider immediate mechanical circulatory support (IABP, Impella, VA-ECMO) in refractory cases at designated Australian ECMO centres.
Ventriculo-Arterial Coupling in Detail
The ratio of ventricular to arterial elastance (Ees/Ea) determines the efficiency of energy transfer from the ventricle to the arterial system:
- Normal coupling (Ees/Ea ≈ 1.0): Maximal stroke work and optimal efficiency (~90% potential energy converted to external work).
- Uncoupling with low Ees (Ees/Ea < 0.6): Systolic heart failure, reduced contractility relative to afterload. Excessive potential energy wasted; poor efficiency.
- Uncoupling with high Ees (Ees/Ea > 1.6): Concentric hypertrophy (e.g., hypertensive heart disease, HOCM). Near-maximal work but reduced adaptability to preload changes; increased myocardial oxygen demand.
Integrated Haemodynamic Profile — Clinical Application
Systematic interpretation of haemodynamics requires integrating pressure, flow, and resistance data:
| Clinical Scenario | CO/CI | PCWP | SVR | Key Feature |
|---|---|---|---|---|
| Cardiogenic shock | ↓↓ (< 2.2) | ↑↑ (> 18) | ↑↑ (> 1500) | Compensatory vasoconstriction |
| Septic shock | ↑ or Normal | ↓ or Normal | ↓↓ (< 800) | Vasoplegia, high output |
| Hypovolaemic shock | ↓↓ | ↓↓ (< 6) | ↑↑ | Low filling pressures |
| Tamponade | ↓↓ | ↑ (equalised) | ↑ | Equalisation of diastolic pressures |
| Acute mitral regurgitation | ↓ (effective CO) | ↑↑ (v waves) | ↑ | Large v waves on PCWP tracing |
| High-output failure | ↑↑ (> 4.0) | ↑ | ↓↓ | Thyrotoxicosis, AV fistula, sepsis |
Aboriginal and Torres Strait Islander Health Considerations
Aboriginal and Torres Strait Islander Health
Special Populations
Paediatric Considerations
Neonatal cardiac output
Normal neonatal CO is ~400–500 mL/kg/min (significantly higher per kg than adults). Neonatal SV is 2–4 mL/beat; CO is highly heart-rate dependent due to limited ability to augment contractility and relatively non-compliant ventricles.
Fractional shortening preference
FS by M-mode is the standard measure of systolic function in paediatric echocardiography. Normal FS 28–44% in children. Simpson's biplane EF is less reliable in small hearts.
Congenital heart disease
In patients with intracardiac shunts (VSD, ASD, PDA), standard CO formulas yield misleading results. Qp/Qs (pulmonary-to-systemic flow ratio) must be calculated: Qp/Qs = (SaO₂ − SvO₂) / (SpvO₂ − SpaO₂). Normal Qp/Qs = 1.0; ratio > 1.5:1 indicates significant left-to-right shunt.
Pregnancy
Normal physiological changes
CO increases 30–50% during pregnancy (peaking at 32 weeks), driven by ↑ HR (15–20 bpm) and ↑ SV (25–30%). SVR decreases by 20–30% due to progesterone-mediated vasodilation and low-resistance placental circulation. MAP decreases in the second trimester then returns toward baseline by term.
Postpartum haemodynamic shift
Autotransfusion at delivery (300–500 mL) causes a transient ↑ CO; CO returns to pre-pregnancy values by 6–12 weeks postpartum. Peripartum cardiomyopathy should be considered if EF < 45% presents in the last month of pregnancy or within 5 months postpartum.
Elderly
Age-related changes
Aging is associated with increased arterial stiffness (↑ Ea), concentric LV remodelling, impaired diastolic relaxation, and blunted chronotropic response to exercise. Resting CO and EF are generally preserved but cardiac reserve (maximum CO during exercise) declines significantly — approximately 1% per year after age 30.
Ventriculo-arterial coupling
In elderly patients, the Ees/Ea ratio is often maintained despite increased Ea by compensatory concentric hypertrophy (↑ Ees). This coupling preserves resting EF but at the cost of diastolic dysfunction, reduced exercise tolerance, and increased susceptibility to pulmonary oedema with volume overload.
Renal Impairment
Cardiorenal interactions
Chronic kidney disease (CKD) promotes volume overload, anaemia (↓ CaO₂), arteriosclerosis (↑ SVR), and uraemic cardiomyopathy. The Fick equation is particularly relevant: in CKD-related anaemia, a widened a-v O₂ difference may mask a low CO. Haemodialysis induces dynamic haemodynamic shifts with significant preload reduction per session.
Immunocompromised
Sepsis-related haemodynamic patterns
Immunocompromised patients are at high risk of sepsis, which produces a characteristic haemodynamic pattern: high CO, low SVR, and low or normal PCWP. Myocardial depression (septic cardiomyopathy) occurs in 40–60% of septic shock cases, with transiently reduced EF that typically recovers over 7–10 days. Differentiating septic cardiomyopathy from primary cardiac pathology requires integration of CO, SVR, and clinical context.
Clinical Application & Interpretation
Quick Reference: Core Formulas
Cardiac Output
CO = HR × SV
4–8 L/min
Cardiac Index
CI = CO / BSA
2.5–4.0 L/min/m²
Fick CO
CO = VO₂ / (CaO₂ − CvO₂)
Gold standard
Ejection Fraction
EF = (EDV − ESV) / EDV × 100
≥ 55%
Fractional Shortening
FS = (LVIDd − LVIDs) / LVIDd × 100
25–45%
MAP
DBP + ⅓(SBP − DBP)
70–105 mmHg
SVR
80 × (MAP − RAP) / CO
800–1200 dyne·s/cm⁵
PVR
80 × (MPAP − PCWP) / CO
< 250 dyne·s/cm⁵
Cardiac Power Output
(MAP × CO) / 451
1.0–1.7 W
Stroke Work
SV × (MAP − PCWP) × 0.0136
5–10 g·m
Stepwise Haemodynamic Assessment
1
Clinical Assessment
Assess perfusion (warm vs cold; capillary refill; urine output; mentation) and congestion (JVP, peripheral oedema, pulmonary crackles). This rapidly categorises patients into four haemodynamic phenotypes.
2
Non-invasive Monitoring
Continuous ECG, pulse oximetry (SpO₂, trending SvO₂ surrogate), non-invasive blood pressure, echocardiography (LV size, EF, valve assessment, IVC collapsibility). Point-of-care ultrasound (POCUS) is increasingly used in Australian emergency departments for rapid haemodynamic assessment.
3
Minimally Invasive CO Monitoring
Arterial waveform analysis (FloTrac/Vigileo, PiCCO, LiDCO) provides continuous CO, SVV, and PPV — valuable in ventilated patients. Available in most Level 5+ ICUs in Australia. Accuracy decreases with irregular rhythms and significant aortic regurgitation.
4
Invasive Haemodynamic Monitoring
PA catheter (Swan–Ganz) for direct measurement of CO (thermodilution or Fick), PCWP, PA pressures, and mixed venous saturation (SvO₂). Reserved for complex or refractory cases. MBS-rebatable in selected clinical scenarios.
Common Pitfalls in Formula Application
- Indexing errors: Always confirm whether the output is indexed (CI, SVI, SWI) or absolute (CO, SV, SW). Mixing these leads to significant misinterpretation.
- Thermodilution in tricuspid regurgitation: Overestimates CO by 20–50%; use Fick method instead.
- FS in regional wall motion abnormalities: One-dimensional measurement may miss dyssynchrony; always correlate with 2D assessment.
- Assumed VO₂ in Fick: Using estimated VO₂ in critically ill patients (e.g., sepsis, burns, hypermetabolic states) introduces significant error; direct calorimetry is preferred.
- SVR in high-output states: Low SVR may be misinterpreted as "good" if CO is not simultaneously elevated.
📚 References
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