12.2 Heart Failure and Cor Pulmonale

Quick Answer: New congestion clusters (weight gain, orthopnoea/PND, oedema, dyspnoea at lower loads) mean modify/stop and medical liaison—not harder training. Stable, compensated HF benefits from carefully titrated exercise using RPE, symptoms, and vitals (HR may be blunted). Cor pulmonale = right-heart strain from lung disease/chronic hypoxia: manage lungs, oxygen, and right-sided congestion together.

Heart failure (HF) appears across acute wards, rehabilitation units, community, and private practice cases on the APC Written Assessment. Cor pulmonale links chronic respiratory disease to right-heart strain. Entry-level physiotherapists must spot decompensation, titrate exercise safely, stop when indicated, liaise on fluid and medical issues, and connect lung disease to right-heart failure—without pretending to adjust loop diuretic doses independently.

Heart Failure: Concepts You Need for Cases

Heart failure is a clinical syndrome in which the heart cannot meet the body’s metabolic needs at normal filling pressures, or can do so only with elevated filling pressures. You will see labels such as HFrEF (reduced ejection fraction), HFpEF (preserved ejection fraction), left-sided, right-sided, and biventricular failure. You do not need research-level echo interpretation. You do need functional implications:

• Reduced cardiac output → fatigue, exercise intolerance, hypotension risk, cool extremities in advanced shock states
• Elevated filling pressures / congestion → pulmonary oedema (dyspnoea, orthopnoea, crackles), systemic venous congestion (oedema, ascites, hepatic congestion)
• Arrhythmias (especially AF) and ischaemia commonly coexist and change exercise risk

NYHA functional classes (I–IV) appear in notes as a rough activity limitation map from no limitation to symptoms at rest. Use them to frame goals, not as the only assessment tool.

Common precipitants of decompensation in vignettes: infection, ischaemia, arrhythmia, non-adherence to fluid/salt/medications, anaemia, renal deterioration, NSAID use, thyrotoxicosis, and progressive valve disease. Physiotherapists often notice the functional decline first during mobility sessions—that observation is clinically valuable when handed over clearly.

Signs of Decompensation You Must Not Miss

Train yourself to cluster symptoms rather than dismiss them one by one:

Dyspnoea

• New or worsening breathlessness at lower workloads than baseline
• Orthopnoea (needing more pillows) and paroxysmal nocturnal dyspnoea (PND)
• Rest dyspnoea or acute respiratory distress with possible pulmonary oedema

Fluid retention

• Peripheral pitting oedema (ankles, legs; sacral in bedbound patients)
• Rapid weight gain (classically ≥1–2 kg over a few days as a red flag pattern taught in HF self-management—confirm local education numbers with team materials)
• Abdominal bloating, ascites, reduced appetite from splanchnic congestion
• Elevated jugular venous pressure signs reported by medical teams; increased work of breathing

Other red clusters

• Marked fatigue, confusion in older adults, reduced urine output themes, cool clammy skin in low-output states
• Productive cough with frothy sputum in acute pulmonary oedema patterns
• Chest pain if ischaemia is driving decompensation
• Syncope or near-syncope with low output or arrhythmia

When these signs appear or worsen during a physiotherapy episode of care, do not “push through for endurance.” Reduce intensity or stop, position for comfort (often upright for pulmonary congestion), monitor SpO2/HR/BP as available, and escalate to nursing/medical review. In community settings, this may mean urgent GP review, hospital ED, or ambulance depending on severity.

Exercise in Heart Failure: Why It Helps and How to Titrate

Stable, compensated HF benefits from structured exercise: improved peripheral muscle efficiency, better symptoms, higher quality of life, and reduced hospitalisation risk in evidence-based programs. Entry-level principles:

1. Confirm relative stability before progressive aerobic training (not acute pulmonary oedema, not uncontrolled arrhythmia, not severe symptomatic hypotension).
2. Start low, progress slow: short bouts of walking or cycle ergometry, frequent rests, build duration before intensity.
3. Use RPE / talk test / symptoms heavily—especially if beta-blocked (blunted HR response).
4. Include lower-limb strength carefully once stable; avoid early heavy isometric straining and breath-holding.
5. Coordinate with HF programs, exercise physiology, and medical parameters (some patients have implantable devices—know ICD/CRT presence conceptually and avoid extreme unilateral shoulder stress early after implant as per device protocols).

Titration example reasoning: if RPE is appropriate, SpO2 holds to target, BP response is reasonable, and recovery is prompt, progress walking time by small increments. If oedema is rising and orthopnoea is worse this week, hold progression and liaise—even if the patient “wants to train hard.”

Interval-style low-level work (walk–rest–walk) often suits limited reserve better than continuous high demand. Home programs must include clear stop rules and when to phone for help. Australian HF and cardiac rehab services increasingly share care with exercise physiologists; collaborative practice—not profession turf wars—is the APC-aligned answer.

When to Stop Exercise in HF (and What to Do Next)

Stop or do not start progressive exercise when you observe or the patient reports:

• Chest pain suggestive of ischaemia
• Severe or rapidly worsening dyspnoea disproportionate to workload
• Dizziness, near-syncope, syncope
• Concerning SpO2 drop below target range with increased work of breathing
• New irregular rapid pulse with symptoms, or known alarming device shocks
• Systolic BP falling significantly with symptoms, or extreme hypertensive response with distress
• Acute neurological change, severe nausea, cold sweat, or confusion
• Failure of HR/symptoms to recover appropriately after rest

Next steps: sit/lie safely as appropriate to the problem (upright often better for pulmonary oedema; supine legs elevated may help pure orthostatic issues—use clinical judgment), monitor, oxygen only if prescribed/protocol, and medical escalation. Document response and modify the plan after medical review. If an ICD fires during a session, treat as a medical event: stop exercise, assess consciousness and symptoms, and follow emergency/medical pathway—do not “reset” devices yourself.

Fluid Status and Medical Liaison

Physiotherapists do not prescribe diuretics, but they are fluid-status observers:

• Ask about daily weights, pillow count, ankle swelling, and nocturnal dyspnoea
• Note sudden weight gain or tight shoes/rings as congestion clues
• Align advice with the HF team’s fluid/salt guidance—do not invent conflicting “drink 4 litres for recovery” messages during acute congestion
• Collaborate when mobility goals conflict with medical priorities (e.g., hold aggressive gym work during IV diuresis for acute decompensated HF)
• Recognise that renal function, electrolytes, and blood pressure limit how hard medical teams can diurese; hypotension after diuresis increases fall and orthostatic risk in your session

Medications you should conceptually respect: ACE inhibitors/ARBs/ARNIs, beta-blockers, mineralocorticoid antagonists, SGLT2 inhibitors, loop diuretics, and device therapy. You need names and side-effect themes (hypotension, bradycardia, hyperkalaemia risk contexts) enough to interpret a vignette, not to prescribe. After aggressive diuresis, expect orthostatic risk and plan staged standing—linking section 12.2 to 12.3.

Cor Pulmonale: The Lung–Right-Heart Link

Cor pulmonale is right ventricular hypertrophy and/or failure secondary to pulmonary hypertension from lung disease or chronic hypoxia, not from primary left-heart failure alone (though overlap exists clinically). Classic associations include advanced COPD, severe interstitial lung disease, chronic thromboembolic disease, and untreated severe sleep-disordered breathing patterns.

Clinical themes:

• Chronic hypoxaemia and hypercapnia drive pulmonary vasoconstriction and vascular remodelling
• Right ventricle faces high afterload → dilatation/failure over time
• Signs of right-sided congestion: peripheral oedema, raised JVP, hepatic congestion, ascites; often with prominent respiratory failure features
• Exercise limited by both ventilatory constraint and cardiac output limit

Physiotherapy implications:

• Prioritise underlying lung management: oxygen therapy as prescribed, airway clearance when indicated, breathing strategies, pulmonary rehab principles, smoking cessation pathways
• Monitor SpO2 carefully; respect oxygen prescription and ambulatory O2 plans
• Expect lower exercise ceilings; titrate with RPE and desaturation rules
• Oedema may be multifactorial (right heart, steroids, immobility, hypoalbuminaemia)—liaise rather than assume “just need more ankle pumps” as sole therapy for massive oedema with rising weight
• Acute worsening of dyspnoea, cyanosis, confusion, or right-heart congestion → medical review for possible decompensation, infection, PE, or progressive respiratory failure

Do not confuse cor pulmonale with primary left HF, but recognise that many patients have mixed disease. Exam answers that only treat “legs oedema with elevation” while ignoring SpO2 84% on air and severe COPD are incomplete.

Setting-Specific Notes

Acute decompensated HF ward: medical stabilisation first; physiotherapy for positioning, early safe mobility when congestion improves, DVT prevention themes, respiratory care, discharge planning.

Outpatient/community HF: progressive exercise, self-management education reinforcement, fall risk with hypotension, caregiver involvement, rapid re-escalation pathways.

Rural/remote: lower threshold to escalate early by phone/telehealth when decompensation signs appear; know local transfer pathways.

Private practice MSK patient with “new ankle swelling and night breathlessness”: do not assume pure venous insufficiency—screen cardiac/respiratory red flags and escalate when the cluster fits decompensation.

APC Traps

• Interpreting new orthopnoea and 3 kg gain as “deconditioning only” and doubling exercise dose
• Ignoring peripheral oedema and fatigue because “they walked yesterday”
• Treating cor pulmonale as pure MSK ankle swelling without oxygen/respiratory reasoning
• Stopping all activity forever in stable HF (exercise is indicated when stable)
• Adjusting diuretics yourself in an MCQ as the first action instead of medical liaison
• Forcing age-predicted HR zones in beta-blocked HF patients

Best answers usually: recognise congestion or instability → modify/stop → liaise → then resume graded exercise in compensated states with monitoring and clear stop rules.

Closing Exam Anchor

Decompensation is a medical problem first; stable HF is an exercise opportunity with careful titration; cor pulmonale keeps lungs and right heart in the same sentence.