• Normal cardiac output ≈ 70 mL/kg/min. For a 70 kg person: CO ≈ 4.9 L/min (~5 L/min). ^[1]
• The heart's job is to match output to metabolic demand. At rest this is ~5 L/min; during exercise it must increase proportionally.

Left heart backward failure (more common) → Pulmonary congestion Right heart backward failure (more common) → Peripheral congestion Left or right heart forward failure (less common) → Syncope, cardiogenic shock ^[1]

The mammalian double circulation means the left and right hearts fail in different directions with different clinical consequences:

The lecture's litre-labelled circulation sketches are conceptual balance sheets. In the normal sketch, venous return and cardiac output are matched at about 5 L/min. In “backward failure,” extra volume accumulates upstream (illustrated as 8 L entering a circuit that still ejects only 5 L), so venous/filling pressure rises. In “forward failure,” output itself falls (illustrated as 8 L upstream but only 3 L ejected), producing both congestion and hypoperfusion. The numbers illustrate mismatch and accumulation, not values to measure at the bedside.

Prior to the optimal point: ↑Venous Return → ↑Stroke Volume/Cardiac Output. After the optimal point: ↑Venous Return → ↓Stroke Volume/Cardiac Output → ↑LVEDV → ↑LVEDP → ↑LA Pressure → ↑Pulmonary Venous Pressure. ^[1]

Why this matters: The Frank-Starling curve is the single most important physiological concept in HF. A normal heart operates on the ascending limb — more stretch = more output. A failing heart has a flattened curve and is pushed past its optimal point. Any additional preload (e.g. lying flat, fluid overload, high-salt diet) no longer increases output; instead, it increases end-diastolic pressure, which transmits backward to the lungs, causing pulmonary congestion and SOB.

The management curve later in the deck reverses that logic: reducing excessive preload can move an overfilled failing ventricle leftward, relieving congestion without sacrificing output, while afterload reduction can improve forward ejection when blood pressure permits. Moving too far left causes underfilling and worsened perfusion — the visual reason to reassess volume and renal function during decongestion.

While lying down, loss of gravitational venous blood pooling results in 300-600 mL increase in venous return to the heart, leading to SOB. While sitting up, partial restoration of gravitational venous blood pooling reduces venous return, resolving orthopnoea. ^[1]

• Orthopnoea: Immediate redistribution of intravascular blood from lower limbs to thorax when supine → overwhelms the failing LV → pulmonary congestion. Relieved within minutes by sitting up.
• PND (Paroxysmal Nocturnal Dyspnoea): Delayed fluid shift from interstitium into circulation over 1-2 hours of lying down → gradual ↑VR → patient wakes gasping. Takes longer to resolve than orthopnoea because the fluid source is interstitial, not intravascular ^[2].

Normal pulmonary capillary hydrostatic pressure ≈ 7 mmHg. Normal plasma oncotic pressure ≈ 28 mmHg. In left heart failure: ↑LVEDP → hydrostatic pressure rises to ~25-30 mmHg → fluid is forced into the interstitium and alveoli. ^[1]

This is a direct application of Starling's equation at the pulmonary capillary. Normally, oncotic pressure (28 mmHg) far exceeds hydrostatic pressure (7 mmHg), keeping alveoli dry. When LV failure raises hydrostatic pressure above oncotic pressure, fluid leaks out → interstitial oedema (Kerley B lines on CXR) → alveolar oedema (batwing opacities, pink frothy sputum).

The lecture references the Framingham Criteria for diagnosing HF. Diagnosis requires 2 major criteria OR 1 major + 2 minor criteria:

Additional Framingham details: A fall in vital capacity by one-third from the maximum recorded value is a minor criterion. Increased circulation time (≥25 seconds) is a major criterion. Weight loss of ≥4.5 kg in 5 days is major when attributable to HF treatment; otherwise it is minor. ^[1]

The Boston Criteria use a scoring system across History, Physical Examination, and CXR criteria. Definite HF: score > 7. Possible HF: 5-7. Unlikely HF: < 5. ^[1]

Key scoring items from the lecture:

This is extremely high-yield for exams. ^[1]

The images on the lecture slides show the progression rather than four unrelated signs: cephalisation → interstitial oedema (Kerley B lines) → perihilar alveolar oedema as filling pressure rises. Kerley B lines are short, horizontal, peripheral basal lines; the bat-wing pattern is central and bilateral. These are teaching correlations, not precise pressure gauges in an individual patient. A normal film does not exclude HF, and portable AP or supine technique can obscure cardiomegaly and vascular redistribution.

The lecture photograph shows the upper level of internal jugular venous pulsation being read vertically above the sternal angle. Start around 30–45° but change the torso angle until the meniscus is visible; 45° is not itself the measurement. Measure the vertical height above the sternal angle (commonly normal up to about 3–4 cm), then add approximately 5 cm to estimate right-atrial pressure. Look for the biphasic, non-palpable waveform and confirm uncertainty with hepatojugular reflux rather than mistaking the carotid pulse for the JVP.

Killip Classification stratifies severity of LV dysfunction and determines clinical status of post-MI patients. ^[1]

B-type natriuretic peptide (BNP) and NT-proBNP are released from the proBNP precursor in response to myocardial wall stress. BNP is the biologically active peptide that signals through NPR-A/cGMP to promote vasodilation and natriuresis; NT-proBNP is an inactive companion fragment used as a biomarker. Neprilysin degrades biologically active natriuretic peptides. ^[1]

Why BNP matters:

• Elevated BNP/NT-proBNP supports a diagnosis of HF, especially when clinical picture is uncertain
• Useful as a rule-out test — a normal BNP makes HF very unlikely (high negative predictive value)
• Should NOT be interpreted in isolation — must be considered alongside all clinical data

Causes for elevated BNP include both cardiac (HF, ACS, valvular disease, AF, myocarditis, LVH) and non-cardiac causes (advancing age, renal failure, anemia, severe pneumonia, pulmonary hypertension, critical illness, sepsis, severe burns). ^[1]

The slide’s diagnostic pathway can be summarised as follows ^[1]:

1. Assess symptoms, past illness and baseline characteristics, family history, physical signs, ECG, and CXR.
2. If one or more findings support possible HF, measure natriuretic peptides. The lecture-era pathway used NT-proBNP ≥400 pg/mL or BNP ≥100 pg/mL to support proceeding to echocardiography.
3. Perform echocardiography, including stress echocardiography when appropriate. If the pathway does not support HF, HF is unlikely.
4. If HF remains uncertain or ischaemic heart disease is still suspected, consider CT, MRI, nuclear cardiology/stress testing, or cardiac catheterisation.
5. Abnormal findings confirm HF and should lead to treatment according to the aetiology and stage; otherwise, prevent HF or arrange follow-up.

Echocardiography is the key investigation for suspected HF. It can identify: pericardial disease (constrictive pericarditis, pericardial effusion), valvular heart diseases (MS/MR, AS/AR), congenital heart diseases (ASD/VSD/PDA), and myocardial disorders (HOCM, HFpEF, HFrEF). ^[1]

Echocardiography tells you:

1. Ejection fraction — distinguishes HFrEF from HFpEF
2. Structural cause — valve disease, wall motion abnormalities (ischaemic), hypertrophy, chamber dilatation
3. Diastolic function/filling pressure — transmitral inflow, tissue Doppler (including E/e′), LA size, TR velocity and the wider clinical context. No single E/A or E/e′ value diagnoses HFpEF by itself.

NYHA classes define the functional limitation of the patient. ^[1]

ACCF/AHA stages capture the progression of HF, including at-risk patients. ^[1]

The lecture's trajectory graph links the stages to changing goals of care:

• Stage A: risk factors but no structural disease — prevent structural heart disease.
• Stage B (pre-HF): structural/functional or biomarker abnormality without HF symptoms — prevent symptomatic HF.
• Stage C: symptoms appear. Function often follows a saw-tooth course: an acute admission causes a steep fall, treatment produces only partial recovery, and repeated episodes lower the baseline.
• Stage D: marked symptoms, recurrent admissions and progressive loss of function despite guideline-directed therapy — evaluate advanced-HF therapies while integrating symptom control and palliative care.

The palliative-care segment should not be read as “care only when treatment stops.” Supportive and advance-care planning can run alongside disease-modifying and device therapy throughout advanced HF ^[14].

This is the most comprehensive list from the lecture and is high-yield. ^[1]

When evaluating a patient with HF, always ask about: established CVD (CAD, PVD, stroke), CV risk factors (HT, smoking, DM, obesity, dyslipidaemia), exposure to cardiotoxic agents (chemotherapy/RT, alcohol, substance abuse), valvular diseases (rheumatic fever, CTD), systemic disorders (thyroid, myopathy, STD, phaeochromocytoma), and family history (CMP, sudden death, myopathy, arrhythmias, premature CVD). ^[1]

1. Is this acute HF? 2. How severe? 3. Any precipitating cause(s)? 4. Hemodynamic subtype? 5. What are the treatment options? ^[1]

The lecture references the ESC/ACC mnemonic. Common precipitants include ^[1]:

• Cardiac: ACS, arrhythmia (especially new AF), valvular emergency, hypertensive crisis
• Systemic: Anaemia, endocrine (thyroid, phaeochromocytoma), adverse drug effects, infection/sepsis, non-compliance with medications or diet (high salt/fluid intake)
• Pulmonary: PE, pneumonia

In suspected acute HF, first assess for cardiogenic shock and respiratory failure:

1. Cardiogenic shock → pharmacological or mechanical circulatory support, with immediate stabilisation and ICU/CCU transfer.
2. Respiratory failure → oxygen for hypoxaemia, non-invasive positive-pressure ventilation (CPAP/BiPAP) for appropriate patients with respiratory distress, or invasive ventilation when non-invasive support fails or is contraindicated.
3. Identify immediately treatable acute aetiologies using CHAMP:
   • C — Acute coronary syndrome
   • H — Hypertensive emergency
   • A — Arrhythmia
   • M — Acute mechanical cause
   • P — Pulmonary embolism
4. If no CHAMP cause is identified, proceed with diagnostic work-up and clinical assessment to select definitive management. ^[1]

Warm & Dry | Warm & Wet | Cold & Dry | Cold & Wet ^[1]

The bedside warm/cold–dry/wet assessment can be applied as follows ^[1]:

• Dry and warm: adequately perfused and approximately compensated → adjust oral therapy.
• Dry and cold: first determine whether the patient is genuinely underfilled; only then consider a cautious fluid challenge. Persistent end-organ hypoperfusion requires urgent reassessment for shock and selective vasoactive support rather than reflex fluids.
• Wet and warm: adequately perfused, often with normal or high systolic BP. Treat significant fluid overload promptly with IV loop diuretic; an IV vasodilator may be added for dyspnoea when systemic hypotension is absent. Escalate the diuretic dose or add a second diuretic if response is inadequate.
• Wet and cold: this is not simply a “low BP” category — look for altered mentation, cool peripheries, oliguria, narrow pulse pressure, raised lactate and other evidence of hypoperfusion. Escalate urgently. Inotrope is for cardiogenic shock/end-organ hypoperfusion, a vasopressor may be required to maintain pressure, and temporary mechanical circulatory support is selected by a shock team when drugs cannot maintain end-organ function ^[14].

The slide's algorithm reflects older teaching (routine bed rest/oxygen/fluid restriction, a nitrate–diuretic–morphine bundle, dopamine for low BP, and automatic progression to IABP). A safer current sequence is:

Key medications in acute HF:

Improve symptoms (congestion and low-output), restore oxygenation, optimize volume status, identify etiology and precipitating factors, optimize chronic oral therapy, minimize side effects, identify candidates for revascularization or device therapy, identify risk of thromboembolism. ^[1]

At least daily: weight (after voiding in AM), fluid I/O, vital signs, signs (oedema, ascites, rales, hepatomegaly, JVP, hepatojugular reflux), symptoms (orthopnoea, PND, dyspnoea, fatigue), electrolytes (K⁺, Na⁺), renal function (BUN, creatinine). ^[1]

1. Relieve symptoms. 2. Improve exercise capacity and QoL. 3. Prevent/treat complications (↓morbidity). 4. Prevent/modify disease progression. 5. Improve prognosis (↓mortality). ^[1]

First and foremost: Treat the underlying cause. ^[1]

Decreased CO → Activation of SNS, RAAS, and vasopressin → ↑HR, ↑contractility, vasoconstriction, ↑circulating volume → Short-term: maintains BP and CO → Long-term: ↑cardiac workload (↑preload and afterload) → Further LV dysfunction → Vicious cycle. ^[1]

This is the vicious cycle of heart failure. The maladaptive neurohormonal activation that initially compensates for ↓CO eventually causes further harm:

• SNS activation → tachycardia, ↑afterload, myocardial oxygen demand, arrhythmias
• RAAS activation → vasoconstriction, Na⁺/H₂O retention, fibrosis, hypertrophy, ↑aldosterone
• Vasopressin → water retention, hyponatraemia

The natriuretic peptide system (ANP/BNP) is a counter-regulatory mechanism that promotes vasodilation, natriuresis, and inhibits RAAS/SNS. However, it is insufficient to overcome the maladaptive activation.

The paradigm shift in HF therapy: from drugs that simply improve haemodynamics (digoxin, diuretics) to drugs that block neurohormonal maladaptation (ACEi, beta-blockers, MRA, ARNI), which actually reduce mortality. ^[1]

The image treats the failing circulation as a tired horse pulling an overloaded wagon. Each intervention solves a different problem:

It is a map of mechanisms, not a treatment sequence. The key modern lesson is to unload congestion while establishing disease-modifying therapy; repeated “whipping” with inotropes can increase arrhythmia and mortality outside a shock, bridge or palliative indication.

The lecture presents the evolution and current standard of care. Offer the four pillars early to patients with HFrEF when indicated and tolerated; dose and sequence depend on blood pressure, renal function, potassium, volume status and comorbidities ^[14]:

ARNI (sacubitril/valsartan = Entresto = LCZ696) is preferred over an ACE inhibitor for suitable symptomatic HFrEF based on PARADIGM-HF:

PARADIGM-HF: LCZ696 (Entresto) vs Enalapril in HFrEF (LVEF < 35%). HR 0.80 for CV mortality/HF hospitalization, NNT = 21. Entresto is now recommended in place of ACEi for eligible HFrEF patients. ^[1]

• PARADIGM-HF: the sacubitril/valsartan event curve separates from enalapril over follow-up, supporting replacement of ACE inhibition by ARNI in eligible symptomatic HFrEF.
• DAPA-HF and EMPEROR-Reduced: the SGLT2-inhibitor curves separate early for the primary composite. The benefit was present with or without diabetes; do not interpret SGLT2 inhibition as merely glucose lowering.
• DAPA-CKD: benefit across diabetes strata reinforces cardiorenal protection, but CKD evidence is not a substitute for checking eGFR, volume status and drug-specific prescribing requirements.
• EMPEROR-Preserved: the composite curve favoured empagliflozin, driven mainly by fewer HF hospitalisations rather than a clearly demonstrated cardiovascular-mortality reduction. The lecture predates further HFpEF/HFmrEF evidence; current ESC guidance recommends an SGLT2 inhibitor for these EF groups ^[15].
• VICTORIA: vericiguat modestly reduced the composite of CV death or first HF hospitalisation in recently worsened high-risk HFrEF, but its CV-death curve did not show a clear stand-alone reduction; it is an additional-agent option, not a fifth universal pillar.

Additional Agents

The lecture presents a powerful timeline showing 1-year mortality reduction through successive drug additions:

• Diuretic + Digoxin alone: ~15%
• • ACEi (SOLVD 1991): 12.8% → RRR 23%
• • Beta-blocker (CIBIS-2 1999): 8.8% → RRR 33%
• • ARNI replacing ACEi (PARADIGM-HF 2013): 7.9% → RRR 16%
• • SGLT2i (DAPA-HF 2019): ~10% → further RRR 17% ^[1]

The lecture's discharge timeline makes a practical point that is easily lost in a drug list: once congestion and haemodynamics have stabilised, start or re-establish the four HFrEF medication classes during hospitalisation when possible, rather than delaying each new class until the previous one reaches target. Continue titration as tolerated and arrange early review of symptoms, volume status, blood pressure, renal function, potassium and adherence. Current US guidance allows low-dose simultaneous or sequential initiation without waiting for one drug to reach target before starting the next ^[14]; the exact schedule must be individualized.

The slide records the historical approach: treat hypertension/CAD and AF, use cautious diuresis for congestion, and consider rate-slowing or RAAS drugs. Current practice is more specific ^[14][15]:

• Use an SGLT2 inhibitor to reduce HF events in eligible HFpEF/HFmrEF patients.
• Use diuretics for clinical congestion; avoid both residual overload and over-diuresis.
• Treat hypertension, AF, ischaemia and important comorbidities such as obesity, diabetes, CKD and sleep-disordered breathing.
• Consider an MRA, ARB or ARNI in selected patients, especially toward the lower end of the preserved-EF spectrum; these are not blanket mortality-reducing substitutes for HFrEF therapy.
• Do not routinely slow sinus rate with a beta-blocker, verapamil or diltiazem solely because the EF is preserved. Use rate/rhythm drugs when there is a separate indication (for example AF, angina or hypertension), and avoid non-dihydropyridine calcium-channel blockers when LV systolic function is reduced.